Wikipedia - Benutzerbeiträge [de]

Grandisol

2016-10-11T20:52:26Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'CASNo_Ref', 'UNII_Ref', 'Verifiedfields') per Chem/infobox_drug validation (report errors or bugs)

{{chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 450502843
| Reference =<ref name="Merck">''[[Merck Index]]'', 11th Edition, '''4442'''</ref><ref name="Science">''Science. '''1969''', ''vol. 166'' pp.1010-1012</ref>
| Name = Grandisol
| ImageFile = Grandisol.png
| ImageSize = 140px
| ImageAlt = Skeletal formula of grandisol
| ImageFile1 = Grandisol 3D ball.png
| ImageSize1 = 160
| ImageAlt1 = Ball-and-stick model of the grandisol molecule
| IUPACName =(+)-2-[(1''R'',2''S'')-1-methyl-2-(prop-1-en-2-yl)cyclobutyl]ethanol
| OtherNames =''cis''-2-Isopropenyl-1-methylcyclobutaneethanol
|Section1={{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 147990
| PubChem = 169202
| InChI = 1/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| InChIKey = SJKPJXGGNKMRPD-VHSXEESVBS
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = SJKPJXGGNKMRPD-VHSXEESVSA-N
| CASNo_Ref = {{cascite|changed|CAS}}
| CASNo = 26532-22-9
| UNII_Ref = {{fdacite|changed|FDA}}
| UNII = 9S44Q9MKXB
| SMILES = OCC[C@]1(C)[C@H](C(=C)C)CC1
}}
|Section2={{Chembox Properties
| Formula = C10H18O
| MolarMass = 154.25 g/mol
| Density =
| MeltingPt=<
| MeltingPtC = 25
| BoilingPtC = 50 to 60
| BoilingPt_notes = at 1 mmHg
}}
}}

'''Grandisol''' is a natural [[organic compound]] with the [[molecular formula]] C10H18O. It is a [[monoterpene]] containing a [[cyclobutane]] ring, an [[alcohol]] group, an [[alkene]] group and two [[Chirality (chemistry)|chiral]] centers (one of which is quaternary).

Grandisol is a [[pheromone]] primarily important as the sex attractant of the [[cotton boll weevil]] (''Anthonomus grandis''), from which it gets its name.<ref name="Merck"/> It is also a pheromone for other related insects. The cotton boll weevil is an agricultural pest that can cause significant economic damage if not controlled. Grandisol is the major constituent of the mixture known as [[grandlure]], which is used to protect cotton crops from the boll weevil.<ref name="Merck"/>

==Synthesis==
Grandisol was first isolated, identified, and synthesized by J. Tumlinson ''et al''. at Mississippi State University in 1969.<ref name="Science"/> The most recent and highest yielding synthetic route to grandisol was reported in January 2010 by a group of chemists at [[Furman University]].<ref>{{cite journal |author1=Graham, Thomas J.A. |author2=Gray, Erin E. |author3=Burgess, James M. |author4=Goess, Brian C. |title=An Efficient Synthesis of (±)-Grandisol Featuring 1,5-Enyne Metathesis |journal=J. Org. Chem. |volume=75 |issue=1 |pages=226–228|date=January 2010 |pmid=19957923|pmc=2798917|doi=10.1021/jo9020375 |url=http://pubs.acs.org/doi/abs/10.1021/jo9020375}}</ref> Though enantioselective syntheses have been reported, racemic grandisol has proven equally effective at attracting boll weevils as the natural enantiomer, rendering moot the need for enantioselective syntheses for agricultural purposes.<ref>{{cite journal |author1=Hibbard, B. |author2=Webster, F. |title=Enantiomeric composition of grandisol and grandisl produced by Pissodes strobi and P. nemorensis and their electroantennogram response to pure enantiomers |journal=J. Chem. Ecol. |volume=19 |issue=10 |pages=2129–2141|date=October 1993 |pmid=|pmc=|doi=10.1007/BF00979652 |url=http://www.springerlink.com/content/n666313620244460/}}</ref>

== References ==
{{reflist}}

[[Category:Insect pheromones]]
[[Category:Alcohols]]
[[Category:Alkenes]]

Triphenylmethylradikal

2016-04-04T22:47:06Z

CheMoBot: Updating {{chembox}} (changes to watched fields) per Chem/Drugbox validation (report errors or bugs)

{{Chembox
| Watchedfields = changed
| verifiedrevid = 462238281
| ImageFile = Triphenylmethylradical.png
| ImageSize = 175
| ImageFile_Ref = {{chemboximage|correct|??}}
| ImageName = Kekulé, skeletal formula of the triphenylmethyl radical
| ImageFile1 = Triphenylmethyl radical ball.png
| ImageAlt1 = Ball-and-stick model of the triphenylmethyl radical
|Section1={{Chembox Identifiers
| ChemSpiderID = 10627185
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| SMILES = c1ccc(cc1)[C](c1ccccc1)c1ccccc1
| SMILES1 = C1=CC=C(C=C1)[C](C1=CC=CC=C1)C1=CC=CC=C1
| StdInChI = 1S/C19H15/c1-4-10-16(11-5-1)19(17-12-6-2-7-13-17)18-14-8-3-9-15-18/h1-15H
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = OHSJPLSEQNCRLW-UHFFFAOYSA-N
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
}}
|Section2={{Chembox Properties
| C=19 | H=15
}}
}}

The '''triphenylmethyl radical''' (often shorted to '''trityl radical''') is a [[persistent radical]] and the first [[radical (chemistry)|radical]] ever described in [[organic chemistry]]. It can be prepared by [[homolysis (chemistry)|homolysis]] of [[triphenylmethyl chloride]] '''1''' (''scheme 1'') by a metal like [[silver]] or [[zinc]] in [[benzene]] or [[diethyl ether]]. The radical '''2''' forms a [[chemical equilibrium]] with the [[quinoid]] type [[Dimer (chemistry)|dimer]] '''3'''([[3-triphenylmethyl-6-diphenylmethylidene-1,4-cyclohexadiene]]). In benzene the concentration of the radical is 2%.<ref>''Advanced Organic Chemistry'' J. March, John Wiley & Sons ISBN 0-471-88841-9</ref>

[[Image:TriphenylmethylRadical.png|400px|center|Scheme 1 Triphenylmethyl radical]]

Solutions containing the radical are [[yellow]] and when the temperature of the solution is raised the yellow color becomes more intense as the equilibrium is shifted in favor of the radical following [[Le Chatelier's principle]].

When exposed to air the radical rapidly oxidizes to the [[peroxide]] (''Scheme 2'') and the color of the solution changes from yellow to colorless. Likewise, the radical reacts with [[iodine]] to triphenylmethyl iodide.

[[Image:Triphenylmethyl radical oxidation.png|300px|center|Scheme 2 Triphenylmethyl radical oxidation]]

The radical was discovered by [[Moses Gomberg]] in 1900.<ref>{{cite journal | title = An instance of trivalent carbon: triphenylmethyl | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1900 | volume = 22 | issue = 11 | pages = 757–771 | doi = 10.1021/ja02049a006}}</ref><ref>{{cite journal | title = On trivalent carbon | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1901 | volume = 23 | issue = 7 | pages = 496–502 | doi = 10.1021/ja02033a015}} (Note: radical is also called a ''cadicle'')</ref><ref>{{cite journal | title = On trivalent carbon | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1902 | volume = 24 | issue = 7 | pages = 597–628 | doi = 10.1021/ja02021a001}}</ref> He tried to prepare [[hexaphenylethane]] from [[triphenylmethyl chloride]] and [[zinc]] in [[benzene]] in a [[Wurtz reaction]] and found that the product, based on its behaviour towards iodine and oxygen, was far more reactive than anticipated.

The correct quinoid structure for the dimer was suggested as early as 1904 but this structure was soon after abandoned by the scientific community in favor of [[hexaphenylethane]] which is structure '''4''' in scheme 1.<ref>{{cite journal | title = The hexaphenylethane riddle | author = J. M. McBride | journal = [[Tetrahedron (journal)|Tetrahedron]] | volume = 30 | issue = 14 | year = 1974 | pages = 2009–2022 | doi = 10.1016/S0040-4020(01)97332-6}}</ref> It subsequently took until 1968 for its rediscovery when researchers at the [[Vrije Universiteit Amsterdam]] published [[proton NMR]] data.<ref>{{cite journal | title = A new interpretation of the monomer-dimer equilibrium of triphenylmethyl- and alkylsubstituted-diphenyl methyl-radicals in solution | author = H. Lankamp, W. Th. Nauta and C. MacLean | journal = [[Tetrahedron Letters]] | volume = 9 | issue = 2 |year = 1968 | pages = 249–254 | doi = 10.1016/S0040-4039(00)75598-5}}</ref>

While the trityl radical forms a quinoid dimer, derivatives thereof with the appropriate substitution pattern do form dimers with a hexaphenylethane structure. X-ray studies give a bond length of 1.67 angstrom for hexakis(3,5-di-''t''-butylphenyl)ethane. Theoretical calculations on a very high level of theory indicate that van-der-Waals attraction between the tert-butyl groups create a potential minimum that is absent in the unsubstituted molecule.<ref>{{Citation |last= Lewars|first=Errol |year=2008 |title=Modeling Marvels |publisher=Springer |chapter=8 – Hexaphenylethane}}</ref><ref>
{{cite journal | doi = 10.1002/anie.201103615 | journal = Angew. Chem. Int. Ed. | volume = 50 | pages = 12639–12642 | year = 2011 | title = Steric crowding can stabilize a labile molecule: Solving the hexaphenylethane riddle | author = Stefan Grimme and Peter R. Schreiner
}}</ref> Other derivatives have been reported as the quinoid dimer <ref>{{cite journal|last1=Uchimura |first1=Y. |last2=Takeda |first2=T. |last3=Katoono |first3=R. |last4=Fujiwara |first4=K. |last5=Suzuki |first5=T. |date=2015 |title=New Insights into the Hexaphenylethane Riddle: Formation of an α,''o''-Dimer. |journal=Angew. Chem. Int. Ed. |doi=10.1002/anie.201500122}}</ref>

==See also==
* [[Triphenylmethyl hexafluorophosphate]]
* [[Triphenylmethane]]
* [[Triphenylmethyl chloride]]
* [[Triphenylmethanol]]
* [[Triarylmethane dye]]
* [[3-triphenylmethyl-6-diphenylmethylidene-1,4-cyclohexadiene]]
* [[hexaphenylethane]]

==References==
{{reflist|2}}

==External links==
* [[Molecule of the Month]] June 1997 [http://www.chm.bris.ac.uk/motm/triphenylmethyl/main1.html Link]
* Experimental procedures [http://www.faidherbe.org/site/cours/dupuis/triphen2.htm Link]

[[Category:Free radicals]]

Benzo(a)fluoranthen

2016-03-16T15:23:38Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'StdInChI_Ref', 'StdInChIKey_Ref') per Chem/Drugbox validation (report errors or bugs)

{{DISPLAYTITLE:Benzo(a)fluoranthene}}
{{correct title|reason=bracket|Benzo[''a'']fluoranthene}}
{{Chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 459952610
| Name = Benzo[''a'']fluoranthene
| ImageFile = Benzo a fluoranthene.png
| ImageSize = 150
| ImageFile1 = Benzo(a)fluoranthene molecule ball.png
| ImageSize1 = 170
| ImageAlt1 = Ball-and-stick model of the benzo[a]fluoranthene molecule
| IUPACName =
| OtherNames =
|Section1={{Chembox Identifiers
| CASNo_Ref = {{cascite|changed|??}}
| CASNo = 203-33-8
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 8792
| InChI =
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C20H12/c1-2-8-15-13(6-1)12-14-7-5-11-17-16-9-3-4-10-18(16)20(15)19(14)17/h1-12H
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = OQDXASJSCOTNQS-UHFFFAOYSA-N
| SMILES = c4cccc5cc1c3c(ccc1)c2ccccc2c3c45
| MeSHName =
}}
|Section2={{Chembox Properties
| Formula =C20H12
| MolarMass =252.3093
| Appearance = Orange-yellow needles
| Density =
| MeltingPtC = 144 to 145
| MeltingPt_notes =
| BoilingPt =
}}
|Section3={{Chembox Hazards
| FlashPt =
}}
}}

'''Benzo[''a'']fluoranthene''' is an organic [[Chemical compound|compound]] with the [[chemical formula]] C20H12.

In February 2014, [[NASA]] announced a [http://www.astrochem.org/pahdb/ greatly upgraded database] for tracking [[polycyclic aromatic hydrocarbons]] (PAHs), including '''Benzo[''a'']fluoranthene''', in the [[universe]]. According to scientists, more than 20% of the [[carbon]] in the universe may be associated with PAHs, possible [[PAH world hypothesis|starting materials]] for the [[Abiogenesis#PAH world hypothesis|formation]] of [[Life#Extraterrestrial life|life]]. PAHs seem to have been formed shortly after the [[Big Bang]], are widespread throughout the universe, and are associated with [[Star formation|new stars]] and [[exoplanets]].<ref name="NASA-20140221">{{cite web |last=Hoover |first=Rachel |title=Need to Track Organic Nano-Particles Across the Universe? NASA's Got an App for That |url=http://www.nasa.gov/ames/need-to-track-organic-nano-particles-across-the-universe-nasas-got-an-app-for-that/ |date=February 21, 2014 |work=[[NASA]] |accessdate=February 22, 2014 }}</ref>

==References ==
{{reflist}}

{{PAHs}}

[[Category:Polycyclic aromatic hydrocarbons]]

{{hydrocarbon-stub}}

Benzamidin

2015-01-22T21:05:31Z

CheMoBot: Updating {{chembox}} (changes to watched fields) per Chem/Drugbox validation (report errors or bugs)

{{Unreferenced stub|auto=yes|date=December 2009}}
{{Chembox
| Watchedfields = changed
| verifiedrevid = 443415204
| ImageFile = Benzamidine.svg| ImageSize = 160px
| ImageName = Skeletal formula
| ImageFile1 = Benzamidine-3D-balls.png
| ImageSize1 = 160px
| ImageName1 = Ball-and-stick model
| IUPACName=Benzenecarboximidamide
| OtherNames=
|Section1={{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2242
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = C01784
| InChI = 1/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| InChIKey = PXXJHWLDUBFPOL-UHFFFAOYAU
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 20936
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = PXXJHWLDUBFPOL-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo=618-39-3
| PubChem=2332
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 41033
| SMILES = [NH]=C(N)c1ccccc1
}}
|Section2={{Chembox Properties
| Formula=C7H8N2
| MolarMass=120.15 g/mol
| Appearance=
| Density=
| MeltingPt=
| BoilingPt=
| Solubility=
}}
|Section3={{Chembox Hazards
| MainHazards=
| FlashPt=
| Autoignition=
}}
}}

'''Benzamidine''' is a reversible [[competitive inhibition|competitive inhibitor]] of [[trypsin]], trypsin-like enzymes and serine proteases.

It is often used as a [[ligand]] in [[protein crystallography]] to prevent [[proteases]] from degrading a protein of interest; the triangular diamine group at the bottom gives it a very obvious 'stick-man' shape which shows up in [[difference density map]]s.

[[Category:Aromatic compounds]]
[[Category:Amidines]]

{{Organic-compound-stub}}

Benzo(a)fluoranthen

2015-01-15T01:37:46Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'CASNo_Ref') per Chem/Drugbox validation (report errors or bugs)

{{DISPLAYTITLE:Benzo(a)fluoranthene}}
{{correct title|reason=bracket|Benzo[''a'']fluoranthene}}
{{Chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 459952610
| Name = Benzo[''a'']fluoranthene
| ImageFile = Benzo a fluoranthene.png
| IUPACName =
| OtherNames =
|Section1={{Chembox Identifiers
| CASNo_Ref = {{cascite|changed|??}}
| CASNo = 203-33-8
| InChIKey = FTOVXSOBNPWTSH-UHFFFAOYAM
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = FTOVXSOBNPWTSH-UHFFFAOYSA-N
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 8792
| InChI =
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C20H12/c1-2-8-15-13(6-1)12-14-7-5-11-17-16-9-3-4-10-18(16)20(15)19(14)17/h1-12H

| SMILES = c4cccc5cc1c3c(ccc1)c2ccccc2c3c45
| MeSHName =
}}
|Section2={{Chembox Properties
| Formula =C20H12
| MolarMass =252.3093
| Appearance = Orange-yellow needles
| Density =
| MeltingPtC = 144 to 145
| Melting_notes =
| BoilingPt =
}}
|Section3={{Chembox Hazards
| FlashPt =
}}
}}

'''Benzo[''a'']fluoranthene''' is an organic [[Chemical compound|compound]] with the [[chemical formula]] C20H12.

In February 2014, [[NASA]] announced a [http://www.astrochem.org/pahdb/ greatly upgraded database] for tracking [[polycyclic aromatic hydrocarbons]] (PAHs), including '''Benzo[''a'']fluoranthene''', in the [[universe]]. According to scientists, more than 20% of the [[carbon]] in the universe may be associated with PAHs, possible [[PAH world hypothesis|starting materials]] for the [[Abiogenesis#PAH world hypothesis|formation]] of [[Life#Extraterrestrial life|life]]. PAHs seem to have been formed shortly after the [[Big Bang]], are widespread throughout the universe, and are associated with [[Star formation|new stars]] and [[exoplanets]].<ref name="NASA-20140221">{{cite web |last=Hoover |first=Rachel |title=Need to Track Organic Nano-Particles Across the Universe? NASA's Got an App for That |url=http://www.nasa.gov/ames/need-to-track-organic-nano-particles-across-the-universe-nasas-got-an-app-for-that/ |date=February 21, 2014 |work=[[NASA]] |accessdate=February 22, 2014 }}</ref>

==References ==
{{reflist}}

{{PAHs}}

[[Category:Polycyclic aromatic hydrocarbons]]

{{hydrocarbon-stub}}

Hinokitiol

2014-11-30T20:15:36Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'ChEBI_Ref', 'Verifiedfields') per Chem/Drugbox validation (report errors or bugs)

{{Chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 415528328
| Reference = <ref>[http://www.sigmaaldrich.com/catalog/ProductDetail.do?N4=469521|ALDRICH&N5=SEARCH_CONCAT_PNO|BRAND_KEY&F=SPEC β-Thujaplicin] at [[Sigma-Aldrich]]</ref>
| ImageFileL1 = beta-thujaplicin.png
| ImageSizeL1 = 150px
| ImageFileR1 = Beta-Thujaplicin-3D-balls.png
| ImageSizeR1 = 160
| ImageAlt1 = Ball-and-stick model
| IUPACName = 2-Hydroxy-6-propan-2-ylcyclohepta-2,4,6-trien-1-one
| OtherNames = β-Thujaplicin; 4-Isopropyltropolone
|Section1={{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 3485
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D04876
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 10447
| InChI = 1/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| InChIKey = FUWUEFKEXZQKKA-UHFFFAOYAT
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 48310
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = FUWUEFKEXZQKKA-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 499-44-5
| PubChem = 3611
| SMILES = O=C1/C=C(\C=C/C=C1/O)C(C)C
}}
|Section2={{Chembox Properties
| C =10|H=12|O=2
| Appearance = Colorless to pale yellow crystals
| Density =
| MeltingPtC = 50 to 52
| Melting_notes =
| BoilingPtC = 140
| Boiling_notes = at 10 mmHg
| Solubility = }}
|Section3={{Chembox Hazards
| MainHazards =
| FlashPtC = 140
| AutoignitionPtC =
}}
}}

'''Hinokitiol''' ('''β-thujaplicin''') is a natural [[Terpenoid|monoterpenoid]] found in the wood of trees in the family [[Cupressaceae]]. It is a [[tropolone]] derivative and one of the [[thujaplicin]]s.<ref>{{cite journal | doi = 10.1139/W08-161 | title = Effects of leaching on fungal growth and decay of western redcedar | year = 2009 | last1 = Chedgy | first1 = Russell J. | last2 = Lim | first2 = Young Woon | last3 = Breuil | first3 = Colette | journal = Canadian Journal of Microbiology | volume = 55 | issue = 5 | pages = 578–86 | pmid = 19483786}}</ref> Hinokitiol has inhibitory effects on ''[[Chlamydia trachomatis]]'' and may be clinically useful as a topical drug.<ref>{{cite journal | doi = 10.1128/AAC.49.6.2519-2521.2005 | url = http://aac.asm.org/cgi/content/full/49/6/2519 | pmid = 15917561 | year = 2005 | last1 = Yamano | first1 = H | last2 = Yamazaki | first2 = T | last3 = Sato | first3 = K | last4 = Shiga | first4 = S | last5 = Hagiwara | first5 = T | last6 = Ouchi | first6 = K | last7 = Kishimoto | first7 = T | title = In vitro inhibitory effects of hinokitiol on proliferation of Chlamydia trachomatis | volume = 49 | issue = 6 | pages = 2519–21 | journal = Antimicrobial agents and chemotherapy | pmc = 1140513}}</ref><ref>Chedgy, Russell. ''Secondary metabolites of Western red cedar (Thuja plicata): their biotechnological applications and role in conferring natural durability''. LAP Lambert Academic Publishing, 2010, ISBN 3-8383-4661-0, ISBN 978-3-8383-4661-8</ref>
The name originates from the fact it was originally isolated in Taiwanese hinoki in 1936.<ref>{{cite journal | doi = 10.1002/tcr.201200024 | last1 = Murata | first1 = I. | last2= Itô |first2 = S. |last3 = Asao |first3 = T. | year = 2012 | title = Tetsuo Nozoe: Chemistry and Life | journal = Chem Record | volume = 12 | issue = 6 | pages = 599–607 | url = http://onlinelibrary.wiley.com/doi/10.1002/tcr.201200024/full}}</ref> It is actually almost absent in japanese hinoki while it is contained in high concentration (about 0.04 of heartwood mass) in Juniperus cedrus, Hiba cedarwood (Thujopsis dolabrata) and Western red cedar (Thuja plicata). It can be readily extracted from the cedarwood with solvent and ultrasonication.<ref>{{cite journal | doi = 10.1515/HF.2007.033 | title = Screening fungi tolerant to Western red cedar (Thuja plicata Donn) extractives. Part 1. Mild extraction by ultrasonication and quantification of extractives by reverse-phase HPLC | year = 2007 | last1 = Chedgy | first1 = Russell J. | last2 = Daniels | first2 = C.R. | last3 = Kadla | first3 = John | last4 = Breuil | first4 = Colette | journal = Holzforschung | volume = 61 | issue = 2 | pages = 190}}</ref>

==References==
{{reflist}}

[[Category:Tropones]]
[[Category:Monoterpenes]]

Benzo(a)fluoranthen

2014-11-28T17:57:30Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'StdInChI_Ref', 'StdInChIKey_Ref', 'Verifiedfields') per Chem/Drugbox validation (report errors or [[user talk:CheMoBot|bug...

{{DISPLAYTITLE:Benzo(a)fluoranthene}}
{{correct title|reason=bracket|Benzo[''a'']fluoranthene}}
{{Chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 459952610
| Name = Benzo[''a'']fluoranthene
| ImageFile = Benzo a fluoranthene.png
| IUPACName =
| OtherNames =
|Section1={{Chembox Identifiers
| InChIKey = FTOVXSOBNPWTSH-UHFFFAOYAM
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = FTOVXSOBNPWTSH-UHFFFAOYSA-N
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 8792
| InChI =
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C20H12/c1-2-8-15-13(6-1)12-14-7-5-11-17-16-9-3-4-10-18(16)20(15)19(14)17/h1-12H

| SMILES = c4cccc5cc1c3c(ccc1)c2ccccc2c3c45
| MeSHName =
}}
|Section2={{Chembox Properties
| Formula =C20H12
| MolarMass =252.3093
| Appearance = Orange-yellow needles
| Density =
| MeltingPtC = 144 to 145
| Melting_notes =
| BoilingPt =
}}
|Section3={{Chembox Hazards
| FlashPt =
}}
}}

'''Benzo[''a'']fluoranthene''' is an organic [[Chemical compound|compound]] with the [[chemical formula]] C20H12.

In February 2014, [[NASA]] announced a [http://www.astrochem.org/pahdb/ greatly upgraded database] for tracking [[polycyclic aromatic hydrocarbons]] (PAHs), including '''Benzo[''a'']fluoranthene''', in the [[universe]]. According to scientists, more than 20% of the [[carbon]] in the universe may be associated with PAHs, possible [[PAH world hypothesis|starting materials]] for the [[Abiogenesis#PAH world hypothesis|formation]] of [[Life#Extraterrestrial life|life]]. PAHs seem to have been formed shortly after the [[Big Bang]], are widespread throughout the universe, and are associated with [[Star formation|new stars]] and [[exoplanets]].<ref name="NASA-20140221">{{cite web |last=Hoover |first=Rachel |title=Need to Track Organic Nano-Particles Across the Universe? NASA's Got an App for That |url=http://www.nasa.gov/ames/need-to-track-organic-nano-particles-across-the-universe-nasas-got-an-app-for-that/ |date=February 21, 2014 |work=[[NASA]] |accessdate=February 22, 2014 }}</ref>

==References ==
{{reflist}}

{{PAHs}}

[[Category:Polycyclic aromatic hydrocarbons]]

{{hydrocarbon-stub}}

Phenylazid

2014-11-26T18:34:31Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'CASNo_Ref', 'Verifiedfields') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chemicals|err...

{{Chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 411095002
| Name = Phenyl azide
| ImageFileL1 = Phenyl-azide-A-2D-skeletal.png
| ImageSizeL1 = 100px
| ImageNameL1 = Skeletal formula
| ImageFileR1 = Phenyl-azide-3D-balls.png
| ImageNameR1 = Ball-and-stick model
| ImageSizeR1 = 125px
| IUPACName = Phenyl azide
| OtherNames = Azidobenzene
|Section1={{Chembox Identifiers
| SMILES = [N-]=[N+]=NC1=CC=CC=C1
| CASNo_Ref = {{cascite|correct|??}}
| CASNo = 622-37-7
| RTECS =
| EINECS = 210-730-3
| EINECSCASNO =
| PubChem = 69319
| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
| ChemSpiderID = 62529
| InChI = 1/C6H5N3/c7-9-8-6-4-2-1-3-5-6/h1-5H
| InChIKey = CTRLRINCMYICJO-UHFFFAOYAH
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C6H5N3/c7-9-8-6-4-2-1-3-5-6/h1-5H
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = CTRLRINCMYICJO-UHFFFAOYSA-N
| MeSHName = C014747
}}
|Section2={{Chembox Properties
| C=6|H=5|N=3
| Appearance = Pale yellow, oily liquid
| Density =
| Solubility = not appreciable
| MeltingPt =
| BoilingPtC = 49 to 50
| BoilingPt = at 5 mmHg
| Viscosity =
}}
|Section7={{Chembox Hazards
| ExternalMSDS =
| MainHazards = explosive
| FlashPt =
| RPhrases =
| SPhrases =
}}
|Section8={{Chembox Related
| Function = compounds
| OtherFunctn = [[Aniline]] [[Nitrobenzene]] [[Nitrosobenzene]] [[Phenylhydrazine]] [[Phenylhydroxylamine]] [[Diazonium compound|Diazonium cation]]
}}
}}

'''Phenylazide''' is an organic compound with the formula C6H5N3. It is one of the prototypical organic azides. It has a pungent odor. The structure consists of a linear [[azide]] substituent bound to a [[phenyl]] group. The C-N=N angle is approximately 120°.

==Preparation==
Phenyl azide is prepared by the [[Diazonium compound|diazotization]] of [[phenylhydrazine]] with [[nitrous acid]]:<ref name=OrgSynth >{{OrgSynth | title = Phenyl azide | author = R. O. Lindsay and C. F. H. Allen | collvol = 3 | collvolpages = 710 | year = 1955 | prep = cv3p0710}}</ref>

:C6H5NHNH2 + HNO2 → C6H5N3 + 2 H2O

Aryl iodides bearing electron-withdrawing substituents undergo metathesis with [[sodium azide]] in the presence of Cu(I), [[sodium ascorbate]], and N,N'-dimethylethane-1,2-diamine (DMEA):
:RC6H4I + NaN3 → RC6H4N3 + NaI

==Chemical reactions==
C6H5N3 is used to make heterocycles via cycloaddition to alkenes and especially [[Azide alkyne Huisgen cycloaddition|alkynes]], particularly those bearing electronegative substituents. It reacts with [[triphenylphosphine]] to give the Staudinger reagent C6H5NP(C6H5)3. Thermolysis induces loss of N2 to give the highly reactive phenylnitrene C6H5N.<ref>W. H. Pearson, P. S. Ramamoorthyin "Phenyl Azide" Encyclopedia of Reagents for Organic Synthesis (Ed: L. Paquette) 2004, J. Wiley & Sons, New York. {{doi|10.1002/047084289}}.</ref>

Phenyl azide and its analogues undergo the [[azide alkyne Huisgen cycloaddition]], a classic example of [[click chemistry]]. For example phenyl azide and [[phenylacetylene]] give diphenyl [[triazole]].

==Safety==
Because of the potential for explosion,<ref name=OrgSynth/> a protective [[blast shield]] is recommended during purification and handling. Distillation temperatures should be as low a possible. ''[[Organic Syntheses]]'' recommends a vacuum of 5mm Hg to give a boiling point of "66–68 °C/21 mm. with a bath temperature of 70–75 °C."<ref name=OrgSynth/> The pure substance may be stored in the dark, cold, and even then the shelf-life is only weeks.

==References==

{{reflist}}

[[Category:Aromatic compounds]]
[[Category:IARC Group 3 carcinogens]]
[[Category:Azides]]

1,2-Bis(dimethylphosphino)ethan

2014-03-12T20:55:32Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields) per Chem/Drugbox validation (report errors or bugs)

{{chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 477203110
| Name = 1,2-Bis(dimethylphosphino)ethane
| OtherNames = DMPE ethylenebis(dimethylphosphine) 1,2-Bis(dimethylphosphino)ethane
| ImageFile = dmpe-2D-skeletal-B.png

| ImageName =
| ImageFile1 = Dmpe-from-xtal-1997-3D-balls.png

| ImageName1 =
| IUPACName = Ethane-1,2-diylbis(dimethylphosphane)
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 124423
| InChI = 1/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| SMILES = P(C)(C)CCP(C)C
| InChIKey = ZKWQSBFSGZJNFP-UHFFFAOYAN
| PubChem = 141059
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = ZKWQSBFSGZJNFP-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|changed|??}}
| CASNo = 23936-60-9
}}
| Section2 = {{Chembox Properties
| Formula = C6H16P2
| MolarMass = 150.14 g mol−1
| BoilingPt = 180 °C
| Density = 0.9 g/mL at 25 °C
}}
| Section4 = {{Chembox Hazards
| GHSPictograms = {{GHS02}}{{GHS07}}<ref name="sigma">{{Sigma-Aldrich|Aldrich|id=261939|name=1,2-Bis(dimethylphosphino)ethane|accessdate=2013-07-20}}</ref>
| EUIndex =
| EUClass =
| RPhrases = {{H-phrases|225|315|319|335}}<ref name="sigma"/>
| SPhrases = {{P-phrases|210|261|305+351+338}}<ref name="sigma"/>
| NFPA-H =
| NFPA-F =
| NFPA-R =
| FlashPt =
| Autoignition =
| LD50 =
}}
}}

'''1,2-Bis(dimethylphosphino)ethane''' ('''dmpe''') is a [[diphosphine ligand]] in [[coordination chemistry]]. It can be synthesised by the reaction of [[Grignard reagent|methylmagnesium iodide]] with 1,2-bis(dichlorophosphino)ethane:<ref>{{cite journal |author=R. J. Burt, J. Chatt, W. Hussain, G. J. Leigh |title=A convenient synthesis of 1,2-bis(dichlorophosphino)ethane, 1,2-bis(dimethylphosphino)ethane and 1,2-bis(diethylphosphino)ethane |journal=[[Journal of Organometallic Chemistry|J. Organomet. Chem.]] |volume=182 |issue=2 |year=1979 |pages=203–6 |doi=10.1016/S0022-328X(00)94383-3}}</ref>

:Cl2PCH2CH2PCl2 + 4MeMgI → Me2PCH2CH2PMe2 + 4MgICl

== References ==
{{reflist}}

{{DEFAULTSORT:Bis(dimethylphosphino)ethane, 1,2-}}
[[Category:Chelating agents]]
[[Category:Bisphosphanes]]

1-Methylimidazol

2014-01-15T17:23:40Z

CheMoBot: Updating {{chembox}} (changes to watched fields) per Chem/Drugbox validation (report errors or bugs)

{{chembox
| Watchedfields = changed
| verifiedrevid = 477207972
| Name = 1-Methylimidazole
| ImageFile= MeIm_main.png
| ImageSize= 100px
| IUPACName = 1-Methylimidazole
| OtherNames = N-Methylimidazole
| Section1 = {{Chembox Identifiers
| SMILES = n1ccn(c1)C
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 113454
| ChemSpiderID = 1348
| InChIKey = MCTWTZJPVLRJOU-UHFFFAOYAU
| SMILES1 = Cn1ccnc1
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 543
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = MCTWTZJPVLRJOU-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 616-47-7
| RTECS =
| InChI = 1/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
}}
| Section2 = {{Chembox Properties
| Formula = C4H6N2
| MolarMass = 82.10 g/mol
| Density = 1.03 g/cm³
| MeltingPt = -6°C
| BoilingPt = 198 °C
| pKa =
}}
| Section7 = {{Chembox Hazards
| EUClass = Harmful (Xn); Corrosive (C)
| ExternalMSDS = [http://msds.chem.ox.ac.uk/ME/1-methylimidazole.html Oxford MSDS] }}
}}

'''1-Methylimidazole''' or '''N-methylimidazole''' is an [[aromatic]] [[heterocyclic]] organic compound with the formula CH3C3H3N2. It is a colourless liquid that is used as a specialty solvent, a base, and as a precursor to some ionic liquids. It is fundamental nitrogen heterocycle and as such mimics for various nucleoside bases as well as histidine and histamine,

==Basicity==
With the N-methyl group, this particular derivative of imidazole cannot tautomerize. It is slightly more basic than imidazole, as indicated by the pKa's of the conjugate acids of 7.0 and 7.4.<ref>Albert, A., Heterocyclic Chemistry, 2nd ed.; 1968 Athlone Press, ISBN 0-485-11092-X</ref> Methylation also provides a significantly lower melting point, which makes 1-methylimidazole a useful solvent.

==Synthesis==
1-Methylimidazole is prepared mainly by two routes industrially. The main one is acid-catalysed methylation of imidazole by methanol. The second method involves the [[Debus-Radziszewski imidazole synthesis|Radziszewski reaction]] from [[glyoxal]], [[formaldehyde]], and a mixture of [[ammonia]] and [[methylamine]].<ref name=Ebel>Ebel, K., Koehler, H., Gamer, A. O., & Jäckh, R. “Imidazole and Derivatives.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2002 Wiley-VCH, {{DOI|10.1002/14356007.a13_661}}</ref><ref>{{cite journal
| title = Ueber die Constitution des Lophins und verwandter Verbindungen
| author = Bronislas Radziszewski
| journal = [[Berichte der deutschen chemischen Gesellschaft]]
| volume = 15
| issue = 2
| pages = 1493–1496
| year = 1882
| url =
| doi = 10.1002/cber.18820150207 }}</ref>

:(CHO)2 + CH2O + CH3NH2 + NH3 → H2C2N(NCH3)CH + 3 H2O

The compound can be synthesized on a laboratory scale by [[methylation]] of imidazole at the [[pyridine]]-like nitrogen and subsequent deprotonation.<ref>Gilchrist, T. L., Heterocyclic Chemistry, 2nd ed.; 1992 Longman Scientific & Technical, ISBN 0-582-06420-1</ref> Similarly, 1-methylimidazole may be synthesized by first deprotonating imidazole to form a sodium salt followed by methylation.<ref>Grimmett, M. R., Imidazole and Benzimidazole Synthesis; 1997 Academic Press, ISBN 0-12-303190-7</ref><ref>Gupta, R. R., Kumar, M., Gupta, V., Heterocyclic Chemistry II: Five Membered Heterocycles; 1999 Springer, ISBN 3-540-65252-3</ref>
:H2C2N(NH)CH + CH3I → [H2C2(NH)(NCH3)CH]I
:H2C2(NH)(NCH3)CH + NaOH → H2C2N(NCH3)CH + H2O + NaI

==Applications==
In the research laboratory, 1-methylimidazole and related derivatives have been used as mimic aspects of diverse imidazole-based biomolecules.

1-Methylimidazole is also the precursor for the synthesis of the methylimidazole monomer of pyrrole-imidazole polyamides. These polymers can selectively bind specific sequences of double-stranded DNA by intercalating in a sequence dependent manner.<ref>Baird, E.E. & Dervan, P.B. J. Am. Chem. Soc. 118 (26), 6141-6146, 1996.</ref>

===Ionic liquid precursor===
1-Methylimidazole alkylates to form dialkyl imidazolium salts. Depending on the alkylating agent and the counteranion, various [[ionic liquid]]s result, e.g. [[1-butyl-3-methylimidazolium hexafluorophosphate]] ("BMIMPF6"):<ref name=Meindersma>Meindersma, W., Maase, M., and De Haan, A. B. “Ionic Liquids.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2007 Wiley-VCH, {{DOI|10.1002/14356007.l14_l01}}</ref><ref>{{OrgSynth | author = Dupont, J., Consorti, C., Suarez, P., de Souza, R. | title = Preparation of 1-Butyl-3-methyl imidazolium-based Room Temperature Ionic Liquids | collvol = 10 | collvolpages = 184 | year = 2004 | prep = v79p0236}}</ref>

:[[File:MeIm IL.png|500px]]

BASF has used 1-methylimidazole as a means to remove acid during their industrial-scale production of diethoxyphenylphosphine. In this biphasic acid scavenging using ionic liquids (BASIL) process, 1-methylimidazole reacts with HCl to produce 1-methylimidazolium chloride, a salt that is easily separated and deprotonated to regenerate 1-methylimidazole.<ref name=Meindersma/>
:2 MeC3N2H3 + C6H5PCl2 + 2 C2H5OH → 2 [MeC3N2H4]Cl + C6H5P(OC2H5)2

==See also==
* [[4-Methylimidazole]]

==References==
{{reflist}}

{{DEFAULTSORT:Methylimidazole, 1-}}
[[Category:Imidazoles]]

Benzo(a)fluoranthen

2013-12-30T06:01:55Z

CheMoBot: Updating {{chembox}} (changes to watched fields - updated 'StdInChI_Ref', 'StdInChIKey_Ref', 'Verifiedfields', 'Watchedfields') per Chem/Drugbox validation (report errors or [[user talk:CheMoBot...

{{DISPLAYTITLE:Benzo(a)fluoranthene}}
{{correct title|reason=bracket|Benzo[''a'']fluoranthene}}
{{Chembox
| Watchedfields = changed
| verifiedrevid = 459952610
|Name = Benzo[''a'']fluoranthene
|ImageFile = Benzo a fluoranthene.png
|IUPACName=
|OtherNames=
|Section1= {{Chembox Identifiers
| InChIKey = FTOVXSOBNPWTSH-UHFFFAOYAM
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = FTOVXSOBNPWTSH-UHFFFAOYSA-N
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 8792
| InChI =
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C20H12/c1-2-8-15-13(6-1)12-14-7-5-11-17-16-9-3-4-10-18(16)20(15)19(14)17/h1-12H
| StdInChIKey = OQDXASJSCOTNQS-UHFFFAOYSA-N
| SMILES = c4cccc5cc1c3c(ccc1)c2ccccc2c3c45
| MeSHName=
}}
|Section2= {{Chembox Properties
| Formula=C20H12
| MolarMass =252.3093
| Appearance= Orange-yellow needles
| Density=
| MeltingPt = 144–145 °C
| BoilingPt =
}}
|Section3= {{Chembox Hazards
| FlashPt=
}}
}}

'''Benzo[''a'']fluoranthene''' is an organic [[Chemical compound|compound]] with the [[chemical formula]] C20H12.

{{PAHs}}

[[Category:Polycyclic aromatic hydrocarbons]]

{{hydrocarbon-stub}}

Ethylazid

2013-07-23T04:47:47Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - updated 'CASNo_Ref') per Chem/Drugbox validation (report errors or bugs)

{{chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 429889878
| ImageFile = Ethyl azide.svg
| ImageSize =
| IUPACName =Azidoethane
| OtherNames = Ethane, azido-; 1-Azidoethane
| Section1 = {{Chembox Identifiers
| CASNo_Ref = {{cascite|changed|??}}
| CASNo = 871-31-8
| UN Number =
| PubChem =79118
| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
| ChemSpiderID = 71449
| SMILES = [N-]=[N+]=N/CC
| InChI = 1/C2H5N3/c1-2-4-5-3/h2H2,1H3
| InChIKey = UCSVJZQSZZAKLD-UHFFFAOYAG
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C2H5N3/c1-2-4-5-3/h2H2,1H3
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = UCSVJZQSZZAKLD-UHFFFAOYSA-N
}}
| Section2 = {{Chembox Properties
| Formula = C2H5N3
| MolarMass = 71.08
| Appearance = liquid
| Density =
| MeltingPt =
| BoilingPt = 50
| Solubility =
| SolubleOther =
}}
| Section3 = {{Chembox Explosive
| ShockSens = High
| FrictionSens = High
| ExplosiveV =
| REFactor = }}
| Section4 = {{Chembox Thermochemistry
| DeltaHc =
| DeltaHf = 266.872
| Entropy =
| HeatCapacity = }}

| Section5 = {{Chembox Hazards
| MainHazards = Harmful, Explosive
| FlashPt =
| Autoignition = }}
| Section8 = {{Chembox Related
| OtherAnions =
| OtherCations =
| OtherFunctn =
| Function =
| OtherCpds = [[Hydrazoic acid]], [[Chlorine azide]], [[Methyl azide]] }}
}}

'''Ethyl azide''' (C2H5N3) is an explosive compound sensitive to rapid heating, shock or impact. It has exploded when heated to room temperature.<ref>{{cite journal | last1 = Campbell | first1 = H. C. | last2 = Rice | first2 = O. K. | title = The Explosion of Ethyl Azide | journal = Journal of the American Chemical Society | year = 1935 | volume = 57 | issue = 6 | pages = 1044–1050 | doi = 10.1021/ja01309a019 }}</ref><ref>{{ cite journal | last1 = Rice | first1 = O. K. | last2 = Campbell | first2 = H. C. | title = The Explosion of Ethyl Azide in the Presence of Diethyl Ether | journal = The Journal of Chemical Physics | year = 1939 | volume = 7 | issue = 8 | pages = 700–709 | doi = 10.1063/1.1750516 }}</ref> When heated to decomposition it emits toxic fumes of [[NOx]].<ref>{{cite journal | last1 = Rice | first1 = O. K. | title = The Role of Heat Conduction in Thermal Gaseous Explosions | journal = The Journal of Chemical Physics | year = 1940 | volume = 8 | issue = 9 | pages = 727–733 | doi = 10.1063/1.1750808 }}</ref><ref>{{cite journal | last1 = Costa Cabral | first1 = B. J. | last2 = Costa | first2 = M. L. | last3 = Almoster Ferreira | first3 = M. A. | title = ChemInform Abstract: Molecular Structure and Ionization Energies of Azides: An ''ab initio'' Study of Hydrazoic Acid, Methyl Azide and Ethyl Azide | journal = ChemInform | year = 2010 | volume = 24 | issue = 37 | pages = no | doi = 10.1002/chin.199337053 }}</ref>

It is irritating to eyes, respiratory system and skin.

==Uses==
Ethyl azide is used in [[organic synthesis]].

==References==
{{reflist}}

[[Category:Azides]]
[[Category:Explosive chemicals]]

1,2-Bis(dimethylphosphino)ethan

2013-07-20T17:29:00Z

CheMoBot: Updating {{chembox}} (changes to verified fields - added verified revid - updated 'CASNo_Ref', 'Verifiedfields', 'Watchedfields', 'verifiedrevid') per Chem/Drugbox validation (report errors or [...

{{chembox
| Verifiedfields = changed
| verifiedrevid = 477203110
| Name = 1,2-Bis(dimethylphosphino)ethane
| OtherNames = DMPE ethylenebis(dimethylphosphine) 1,2-Bis(dimethylphosphino)ethane
| ImageFile = dmpe-2D-skeletal-B.png

| ImageName =
| ImageFile1 = Dmpe-from-xtal-1997-3D-balls.png

| ImageName1 =
| IUPACName = Ethane-1,2-diylbis(dimethylphosphane)
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 124423
| InChI = 1/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| SMILES = P(C)(C)CCP(C)C
| InChIKey = ZKWQSBFSGZJNFP-UHFFFAOYAN
| PubChem = 141059
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = ZKWQSBFSGZJNFP-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|changed|??}}
| CASNo = 23936-60-9
}}
| Section2 = {{Chembox Properties
| Formula = C6H16P2
| MolarMass = 150.14 g mol−1
| BoilingPt = 180 °C
| Density = 0.9 g/mL at 25 °C
}}
| Section4 = {{Chembox Hazards
| GHSPictograms = {{GHS02}}{{GHS07}}<ref name="sigma">{{Sigma-Aldrich|Aldrich|id=261939|name=1,2-Bis(dimethylphosphino)ethane|accessdate=2013-07-20}}</ref>
| EUIndex =
| EUClass =
| RPhrases = {{H-phrases|225|315|319|335}}<ref name="sigma"/>
| SPhrases = {{P-phrases|210|261|305+351+338}}<ref name="sigma"/>
| NFPA-H =
| NFPA-F =
| NFPA-R =
| FlashPt =
| Autoignition =
| LD50 =
}}
}}

'''1,2-Bis(dimethylphosphino)ethane''' ('''dmpe''') is a [[diphosphine ligand]] in [[coordination chemistry]]. It can be synthesised by the reaction of [[Grignard reagent|methylmagnesium iodide]] with 1,2-bis(dichlorophosphino)ethane:<ref>{{cite journal |author=R. J. Burt, J. Chatt, W. Hussain, G. J. Leigh |title=A convenient synthesis of 1,2-bis(dichlorophosphino)ethane, 1,2-bis(dimethylphosphino)ethane and 1,2-bis(diethylphosphino)ethane |journal=[[Journal of Organometallic Chemistry|J. Organomet. Chem.]] |volume=182 |issue=2 |year=1979 |pages=203–6 |doi=10.1016/S0022-328X(00)94383-3}}</ref>

:Cl2PCH2CH2PCl2 + 4MeMgI → Me2PCH2CH2PMe2 + 4MgICl

== References ==
{{reflist}}

{{DEFAULTSORT:Bis(dimethylphosphino)ethane, 1,2-}}
[[Category:Chelating agents]]
[[Category:Bisphosphanes]]

Ethylazid

2013-06-18T03:04:39Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - added verified revid - updated 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'Verifiedfields', 'Watchedfields', 'verifiedrevid') per Chem/Drugbox validation (repor...

{{chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 429889878
| ImageFile = Ethyl azide.svg
| ImageSize =
| IUPACName =Azidoethane
| OtherNames = Ethane, azido-; 1-Azidoethane
| Section1 = {{Chembox Identifiers
| CAS No 871-31-8
| UN Number =
| PubChem =79118
| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
| ChemSpiderID = 71449
| SMILES = [N-]=[N+]=N/CC
| InChI = 1/C2H5N3/c1-2-4-5-3/h2H2,1H3
| InChIKey = UCSVJZQSZZAKLD-UHFFFAOYAG
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C2H5N3/c1-2-4-5-3/h2H2,1H3
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = UCSVJZQSZZAKLD-UHFFFAOYSA-N
}}
| Section2 = {{Chembox Properties
| Formula = C2H5N3
| MolarMass = 71.08
| Appearance = liquid
| Density =
| MeltingPt =
| BoilingPt = 50
| Solubility =
| SolubleOther =
}}
| Section3 = {{Chembox Explosive
| ShockSens = High
| FrictionSens = High
| ExplosiveV =
| REFactor = }}
| Section4 = {{Chembox Thermochemistry
| DeltaHc =
| DeltaHf = 266.872
| Entropy =
| HeatCapacity = }}

| Section5 = {{Chembox Hazards
| MainHazards = Harmful, Explosive
| FlashPt =
| Autoignition = }}
| Section8 = {{Chembox Related
| OtherAnions =
| OtherCations =
| OtherFunctn =
| Function =
| OtherCpds = [[Hydrazoic acid]], [[Chlorine azide]], [[Methyl azide]] }}
}}

'''Ethyl azide''' (C2H5N3) is an explosive compound sensitive to rapid heating, shock or impact. It has exploded when heated to room temperature.<ref>{{cite journal | last1 = Campbell | first1 = H. C. | last2 = Rice | first2 = O. K. | title = The Explosion of Ethyl Azide | journal = Journal of the American Chemical Society | year = 1935 | volume = 57 | issue = 6 | pages = 1044–1050 | doi = 10.1021/ja01309a019 }}</ref><ref>{{ cite journal | last1 = Rice | first1 = O. K. | last2 = Campbell | first2 = H. C. | title = The Explosion of Ethyl Azide in the Presence of Diethyl Ether | journal = The Journal of Chemical Physics | year = 1939 | volume = 7 | issue = 8 | pages = 700–709 | doi = 10.1063/1.1750516 }}</ref> When heated to decomposition it emits toxic fumes of [[NOx]].<ref>{{cite journal | last1 = Rice | first1 = O. K. | title = The Role of Heat Conduction in Thermal Gaseous Explosions | journal = The Journal of Chemical Physics | year = 1940 | volume = 8 | issue = 9 | pages = 727–733 | doi = 10.1063/1.1750808 }}</ref><ref>{{cite journal | last1 = Costa Cabral | first1 = B. J. | last2 = Costa | first2 = M. L. | last3 = Almoster Ferreira | first3 = M. A. | title = ChemInform Abstract: Molecular Structure and Ionization Energies of Azides: An ''ab initio'' Study of Hydrazoic Acid, Methyl Azide and Ethyl Azide | journal = ChemInform | year = 2010 | volume = 24 | issue = 37 | pages = no | doi = 10.1002/chin.199337053 }}</ref>

It is irritating to eyes, respiratory system and skin.

==Uses==
Ethyl azide is used in [[organic synthesis]].

==References==
{{reflist}}

[[Category:Azides]]
[[Category:Explosive chemicals]]

1-Methylimidazol

2012-02-19T07:59:02Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors or bugs)

{{chembox
| verifiedrevid = 477207972
| Name = '''1-Methylimidazole'''
| ImageFile= MeIm_main.png
| ImageSize= 100px
| IUPACName = 1-Methylimidazole
| OtherNames = N-Methylimidazole
| Section1 = {{Chembox Identifiers
| SMILES = n1ccn(c1)C
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 113454
| ChemSpiderID = 1348
| InChIKey = MCTWTZJPVLRJOU-UHFFFAOYAU
| SMILES1 = Cn1ccnc1
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 543
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = MCTWTZJPVLRJOU-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 616-47-7
| RTECS =
| InChI = 1/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
}}
| Section2 = {{Chembox Properties
| Formula = C4H6N2
| MolarMass = 82.10 g/mol
| Density = 1.03 g/cm³
| MeltingPt = -60 °C
| BoilingPt = 198 °C
| pKa =
}}
| Section7 = {{Chembox Hazards
| EUClass = Harmful (Xn); Corrosive (C)
| ExternalMSDS = [http://msds.chem.ox.ac.uk/ME/1-methylimidazole.html Oxford MSDS] }}
}}

'''1-Methylimidazole''' or '''N-Methylimidazole''' is an [[aromatic]] [[heterocyclic]] organic compound with the formula CH3C3H3N2. Its N-methylation removes the possibility of tautomerization, which occurs in [[imidazole]] and many imidazole derivatives. 1-Methylimidazole maintains the pyridine-like nitrogen of imidazole, only with a slightly higher pKa.<ref>Albert, A., Heterocyclic Chemistry, 2nd ed.; 1968 Athlone Press, ISBN 048511092X</ref> The methylation also provides a significantly lower melting point, which makes 1-methylimidazole a useful solvent.

1-Methylimidazole has found use as a solvent, a base, a catalyst, a mimic for purine nucleoside bases and histidine and histamine, and as an ionic liquid precursor.

[[Image:MeIm pKa.png|500px]]

==Synthesis==

1-Methylimidazole is synthesized on an industrial scale by the [[Debus-Radziszewski imidazole synthesis|Radziszewski reaction]] from [[glyoxal]], [[formaldehyde]], and a mixture of [[ammonia]] and [[methylamine]].<ref name=Ebel>Ebel, K., Koehler, H., Gamer, A. O., & Jäckh, R. “Imidazole and Derivatives.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2002 Wiley-VCH, {{DOI|10.1002/14356007.a13_661}}</ref><ref>{{cite journal
| title = Ueber die Constitution des Lophins und verwandter Verbindungen
| author = Bronislas Radziszewski
| journal = [[Berichte der deutschen chemischen Gesellschaft]]
| volume = 15
| issue = 2
| pages = 1493–1496
| year = 1882
| url =
| doi = 10.1002/cber.18820150207 }}</ref>

:[[Image:MeIm Rad rxn.png|500px]]

The compound can also be synthesized on a laboratory scale by [[methylation]] of imidazole at the [[pyridine]]-like nitrogen and subsequent deprotonation.<ref>Gilchrist, T. L., Heterocyclic Chemistry, 2nd ed.; 1992 Longman Scientific & Technical, ISBN 0-582-06420-1</ref> Similarly, 1-methylimidazole may be synthesized by first deprotonating imidazole to form a sodium salt followed by methylation.<ref>Grimmett, M. R., Imidazole and Benzimidazole Synthesis; 1997 Academic Press, ISBN 0-12-303190-7</ref><ref>Gupta, R. R., Kumar, M., Gupta, V., Heterocyclic Chemistry II: Five Membered Heterocycles; 1999 Springer, ISBN 3-540-65252-3</ref>

:[[Image:MeIm me rxn.png|500px]]

==Biomolecule analog==
The imidazole backbone is an essential functional unit in biology. The amino acid histidine, the signaling molecule histamine, and the purine nucleobases all contain an imidazole ring.<ref name=Ebel/>

[[Image:MeIm bio.png|500px]]

1-Methylimidazole and its derivatives have been used to mimic aspects of these biomolecules. These mimics can be useful in studies to elucidate biological mechanisms and as portions of synthetic bioactive molecules.

1-Methylimidazole is also the precursor for the synthesis of the methylimidazole monomer of pyrrole-imidazole polyamides. These polymers can selectively bind specific sequences of double-stranded DNA by intercalating in a sequence dependent manner.<ref>Baird, E.E. & Dervan, P.B. J. Am. Chem. Soc. 118 (26), 6141-6146, 1996.</ref>

==Ionic liquid precursor==
1-Methylimidazole alkylates to form dialkyl imidazolium salts. Depending on the alkylating agent and the counteranion, various [[ionic liquid]]s result, e.g. [[1-butyl-3-methylimidazolium hexafluorophosphate]] ("BMIMPF6"):<ref name=Meindersma>Meindersma, W., Maase, M., and De Haan, A. B. “Ionic Liquids.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2007 Wiley-VCH, {{DOI|10.1002/14356007.l14_l01}}</ref><ref>{{OrgSynth | author = Dupont, J., Consorti, C., Suarez, P., de Souza, R. | title = Preparation of 1-Butyl-3-methyl imidazolium-based Room Temperature Ionic Liquids | collvol = 10 | collvolpages = 184 | year = 2004 | prep = v79p0236}}</ref>

:[[Image:MeIm IL.png|500px]]

BASF has used 1-methylimidazole as a means to remove acid during their industrial-scale production of diethoxyphenylphosphine. In this biphasic acid scavenging using ionic liquids (BASIL) process, 1-methylimidazole reacts with HCl to produce 1-methylimidazolium chloride, a salt that is easily separated and deprotonated to regenerate 1-methylimidazole.<ref name=Meindersma/>
:2 MeC3N2H3 + C6H5PCl2 + 2 C2H5OH → 2 [MeC3N2H4]Cl + C6H5P(OC2H5)2

==References==
{{reflist}}

{{DEFAULTSORT:Methylimidazole, 1-}}
[[Category:Imidazoles]]

Natriumthiopental

2012-02-19T07:39:13Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - added verified revid - updated '') per Chem/Drugbox validation (report errors or bugs)

{{drugbox
| Verifiedfields = changed
| verifiedrevid = 476993112
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = Sodium thiopental.svg
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| Drugs.com = {{drugs.com|monograph|thiopental-sodium}}
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1–2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= }}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= }}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 9561
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|changed|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|changed|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web | year = March 2005 | url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf | title = WHO Model List of Essential Medicines | format = PDF | publisher = World Health Organization | accessdate = 2006-03-12}}</ref> It is also usually the first of three drugs administered during most [[lethal injection]]s in the United States.


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1–2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18 |author-separator=, |author2=Barceló B |author3=Homar J |display-authors=3 |last4=Abadal |first4=JM |last5=Molina |first5=FJ |last6=De La Peña |first6=A |last7=Sahuquillo |first7=J |last8=Ibáñez |first8=J}}</ref> in reducing intracranial pressure.This phenomena is also termed as Reverse steal Effect.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, objected to the use of thiopental in lethal injection. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental is questionable.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help relieve trauma in surviving victims of the [[Holocaust]].<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
Thiopental rapidly and easily crosses the blood brain barrier as it is a lipophillic molecule. As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue, due to its very high fat:water partition coefficient (aprx 10), leading to sequestration in fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |author-separator=, |author2=Chantin C |author3=Boulieu R |display-authors=3 |last4=Cotte |first4=J |last5=Berthier |first5=JC |last6=Fraisse |first6=D |last7=Bobenrieth |first7=MJ}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary edema]] in rats. This pulmonary edema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |author-separator=, |author2=Gómez-Cambronero L |author3=Alberola A |display-authors=3 |last4=Fabregat |first4=G |last5=Cerdá |first5=M |last6=Escobar |first6=J |last7=Sabater |first7=L |last8=García-De-La-Asuneión |first8=J |last9=Viña |first9=J}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as [[Hospira]].

Thiopental is famously associated with a number of anesthetic deaths in victims of the [[attack on Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through [[freedom of information legislation]] and has been reviewed in the ''[[British Journal of Anaesthesia]]''.<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base.
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==See also==
* [[Pentobarbital]]

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
[[de:Thiopental]]
[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fa:تیوپنتال]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Icean

2012-02-12T21:22:03Z

CheMoBot: Updating {{chembox}} (changes to verified and watched fields - added verified revid - updated 'ChemSpiderID_Ref', 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'CASNo_Ref') per [[WP:CHEMVALID...

{{chembox
| Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 424837516
| Name = Iceane
| ImageFileL1 = Iceane-3D-sticks.png
| ImageSizeL1 = 100px
| ImageFileR1 = Iceane-3D-vdW.png
| ImageSizeR1 = 100px
| IUPACName = Tetracyclo[5.3.1.12,604,9]dodecane
| OtherNames = Wurtzitane
| Section1 = {{Chembox Identifiers
| CASNo_Ref = {{cascite|correct|??}}
| CASNo = 53283-19-5
| RTECS =
| ChemSpiderID_Ref = {{chemspidercite|changed|chemspider}}
| ChemSpiderID = 26333278
| SMILES = C1C2CC3CC1C4CC2CC3C4
| InChI = 1/C12H18/c1-7-2-11-3-8(1)10-4-9(7)5-12(11)6-10/h7-12H,1-6H2/t7-,8+,9+,10-,11-,12+
| InChIKey = KZNNISMAUNEBPT-KUDAMMAABM
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| StdInChI = 1S/C12H18/c1-7-2-11-3-8(1)10-4-9(7)5-12(11)6-10/h7-12H,1-6H2/t7-,8+,9+,10-,11-,12+
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = KZNNISMAUNEBPT-KUDAMMAASA-N
}}
| Section2 = {{Chembox Properties
| Formula = C12H18
| MolarMass = 163.56 g/mol
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}}

'''Iceane''' is a [[saturated hydrocarbon|saturated]] [[polycyclic compound|polycyclic]] [[hydrocarbon]] with formula C12H18. It has a [[Cage (enclosure)|cage]]-like [[molecule|molecular]] structure, whose [[carbon]] skeleton can be viewed as three fused [[cyclohexane]] rings in the "boat" [[cyclohexane conformation|conformation]]; or as two such rings in the "chair" conformation, connected by three parallel bonds.

The name "iceane" was proposed by the chemist [[Louis Fieser]] about a decade before the compound was first prepared. He was carrying out studies on the arrangement of [[water]] molecules in [[ice]], when it occurred to him that there could exist a stable hydrocarbon with the above structure.{{Fact|date=November 2009}}

It is also referred to as '''wurtzitane''',<ref>[[DOI: 10.1002/hlca.19750580522]]</ref> due to its similarity to the [[wurtzite crystal structure]];<ref>[[doi:10.1071/CH9761721]]</ref> however, the name "iceane" has precedence.

==See also==
* [[Adamantane]]
* [[Twistane]]
* [[Propellane]]
* [[Hexanitrohexaazaisowurtzitane]]

==References==
{{Reflist}}

==External links==
*[http://www.rsc.org/publishing/journals/article.asp?doi=C39820000372 Royal Society of Chemistry Journal]
*[http://books.google.co.uk/books?id=U-VW1MPrX0UC&pg=PA129&lpg=PA129&dq=iceane&source=web&ots=rDYPei2_Rx&sig=utmV9O3nTJcYeyEP8DJDRHW87a0&hl=en#PPA129,M1 ''Symmetry Through the Eyes of a Chemist'', Magdolna Hargittai]
*[http://books.google.com/books?id=7kvAOwqRU0sC&pg=PA68&dq=iceane&ei=COHTR_32IJGgygTghPyABA&sig=u38TtPLJfOn1kO8X4FQ9Ph-5-KI#PPA68,M1Symmetry: ''A Basis for Synthesis Design'', Tse-Lok Ho]
*[http://books.google.co.uk/books?id=2sSMEMkarFkC&pg=PA154&lpg=PA154&dq=iceane+CAS+rn&source=web&ots=C1kQeVJ9IQ&sig=JiACJW1L595tHxO9a91NSP_lqF4&hl=en#PPA154,M1 ''Structures and Energies of Polycyclic Hydrocarbons'', Joan E. Shields]

[[Category:Cycloalkanes]]

{{Organic-compound-stub}}

[[ja:アイサン]]

Pentosanpolysulfat-Natrium

2011-12-30T16:17:57Z

CheMoBot: Updating {{drugbox}} (changes to watched fields - added verified revid - updated 'ChemSpiderID_Ref', 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'CAS_number_Ref') per [[WP:CHEMVALID|Chem/Dr...

{{Drugbox
| Watchedfields = changed
| verifiedrevid = 464198430
| IUPAC_name =
| image = Pentosan polysulfate.svg
| width = 150px


| tradename =
| Drugs.com = {{drugs.com|CDI|pentosan_polysulfate}}
| pregnancy_category = B
| legal_status =
| routes_of_administration = [[mouth|Oral]], [[intramuscular injection|intramuscular]], [[intra-articular]], [[intraventricular]]


| bioavailability =
| metabolism =
| elimination_half-life =
| excretion = Urine


| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = NA
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 37300-21-3
| CAS_supplemental = (free acid) {{CAS|116001-96-8}} (sodium salt)
| ATC_prefix = C05
| ATC_suffix = BA04
| ATC_supplemental = {{ATC|G04|BX15}} {{ATCvet|M01|AX90}}
| PubChem = 37720


| chemical_formula = (C5H6Na2O10S2)n
| molecular_weight =
}}
'''Pentosan polysulfate''' (sold under the name '''Elmiron''' by [[Ortho-McNeil Pharmaceutical]]) is the only oral medication approved by the U.S. FDA for the treatment of [[interstitial cystitis]], also known as painful bladder syndrome.

==Uses==
===Interstitial cystitis/painful bladder syndrome===
[[Interstitial cystitis/painful bladder syndrome]] (IC/PBS) patients struggle with symptoms of urinary frequency, urgency, pressure and/or pain, as well as nocturia (frequent urination at night), dyspareunia (painful intercourse), pain and/or discomfort while sitting in a car, while driving and/or travelling.

The origin/cause of IC/PBS is unknown though a number of theories are currently under consideration. Urine cultures are typically negative for infection, yet it is not unusual for patients to believe that they have had infections for years rather than IC/PBS, because the symptoms of an infection are nearly identical to the symptoms of IC/PBS.

Pentosan polysulfate is available as pills or directly infused into the bladder.

===Transmissible spongiform encephalopathies===
Recently pentosan polysulfate has gained attention as possibly being effective in the treatment of [[Creutzfeldt-Jakob disease]] (CJD), although there is as yet no definitive evidence for this other than results of the ongoing treatment (published) of one patient in Northern Ireland and around six other patients in mainland Britain.<ref>[http://news.bbc.co.uk/1/hi/health/4306351.stm BBC NEWS | Health | Research will now assess CJD drug]</ref>

Around 15 other patients in non-UK countries have also received this treatment in an attempt to halt or slow down CJD and related disease progression.

===Osteoarthrosis in adult dogs===
Recently PPN is being marketed as an alternative for the treatment of lameness and pain of degenerative joint disease/osteoarthrosis (non-infectious arthrosis) in the skeletally mature dog.

'''Cartrophen-Vet''' is a 100mg/ml formulation of Pentosan polysulphate that has been used in Australia since the early 1990s. It is produced by Biopharm Australia [http://www.r-biopharm.com/distributors_content.php?language=english&cid=10004&sub=1&conti=Oceania&country=Australia&].

3 mg/kg PPN is given subcutaneously every 5-7 days for 4 treatments. Subsequent single booster shots are usually given every 3-6 months. <ref>[http://www.vmd.gov.uk/espcsite/Documents/176337.DOC]</ref>

==Pharmacology==
Pentosan is believed to work by providing a protective coating to the damaged bladder wall. The critical flaw of the medication, however, is its exceptionally poor bioavailability when taken orally. Research presented late in 2005 by Alza Pharmaceuticals demonstrates that more than 94% of the medication is excreted, intact, in feces without providing any beneficial effect.<ref>Simon M, McClanahan RH, Shah JF et al. Metabolism of [3H]pentosan polysulfate sodium (PPS) in healthy human volunteers. Xenobiotica. 2005 Aug;35(8):775-84. PMID 16278190</ref> Their research found that only 6% was excreted through urine. The drug must be taken for several months for most patients to achieve some benefit.

More recently, however, pentosan polysulfate has been studied as part of a "rescue instillation" which is placed directly in the bladder and can, perhaps, provide better effectiveness. C. Lowell Parsons has presented a research study which shows a 90% effectiveness in reducing the symptoms of IC/PBS patients by using this instillation.{{Citation needed|date=January 2008}}

==Side effects==
{{Unreferenced section|date=August 2011}}
Patients who have taken pentosan orally report a variety of side effects, primarily GI complaints such as diarrhea, heartburn, stomach pain. Hair loss, headache, rash, insomnia have also been reported. One concern is the potential for increased blood coagulation times with this medication. Some patients have reported that they bruise more easily. In some cases, patients are asked to stop medication before any major surgical procedures to reduce the likelihood of bleeding.

==References==
{{Reflist}}

==External links==
* [http://www.ic-network.com/guestlectures/ "Meet the IC Expert" Guest Lecture by C. Lowell Parsons, MD]
* [http://www.orthoelmiron.com/ic-faqs.html Elmiron FAQ] (For Interstitial Cystitis patients)
* {{PDF|1=[http://www.myortho360.com/myortho360/assets/elmiron/Elmiron_PI.pdf Prescribing Information]}}.

{{Vasoprotectives}}
{{Urologicals, including antispasmodics}}

[[Category:Drugs]]
[[Category:Urologic pelvic pain syndrome]]

[[es:Pentosano polisulfato]]

Hinokitiol

2011-12-11T03:23:01Z

CheMoBot: Updating {{chembox}} (changes to watched fields - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report errors or bugs)

{{Chembox
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| Reference = <ref>[http://www.sigmaaldrich.com/catalog/ProductDetail.do?N4=469521|ALDRICH&N5=SEARCH_CONCAT_PNO|BRAND_KEY&F=SPEC β-Thujaplicin] at [[Sigma-Aldrich]]</ref>
| ImageFile = beta-thujaplicin.png
| ImageSize = 150px
| IUPACName = 2-Hydroxy-6-propan-2-ylcyclohepta-2,4,6-trien-1-one
| OtherNames = β-Thujaplicin; 4-Isopropyltropolone
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
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| KEGG_Ref = {{keggcite|correct|kegg}}
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| InChI = 1/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| InChIKey = FUWUEFKEXZQKKA-UHFFFAOYAT
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 48310
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| StdInChI = 1S/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = FUWUEFKEXZQKKA-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 499-44-5
| PubChem = 3611
| SMILES = O=C1/C=C(\C=C/C=C1/O)C(C)C
}}
| Section2 = {{Chembox Properties
| C=10|H=12|O=2
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| BoilingPt = 140 °C at 10 mmHg
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| Section3 = {{Chembox Hazards
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| Autoignition = }}
}}

'''Hinokitiol''' ('''β-thujaplicin''') is a natural [[Terpenoid|monoterpenoid]] found in the wood of trees in the family [[Cupressaceae]]. It is a [[tropolone]] derivative and one of the [[thujaplicin]]s<ref>Chedgy, Russell et al. ''Effects of leaching on fungal growth and decay of Western red cedar (Thuja plicata)''. Canadian Journal of Microbiology 55(5): 578-586, 2009, DOI: 10.1139/W08-161</ref>. Hinokitiol has inhibitory effects on ''[[Chlamydia trachomatis]]'' and may be clinically useful as a topical drug.<ref>{{cite journal | doi = 10.1128/AAC.49.6.2519-2521.2005 | url = http://aac.asm.org/cgi/content/full/49/6/2519 | pmid = 15917561 | year = 2005 | last1 = Yamano | first1 = H | last2 = Yamazaki | first2 = T | last3 = Sato | first3 = K | last4 = Shiga | first4 = S | last5 = Hagiwara | first5 = T | last6 = Ouchi | first6 = K | last7 = Kishimoto | first7 = T | title = In vitro inhibitory effects of hinokitiol on proliferation of Chlamydia trachomatis | volume = 49 | issue = 6 | pages = 2519–21 | journal = Antimicrobial agents and chemotherapy | pmc = 1140513}}</ref><ref>Chedgy, Russell. ''Secondary metabolites of Western red cedar (Thuja plicata): their biotechnological applications and role in conferring natural durability''. LAP Lambert Academic Publishing, 2010, ISBN-10: 3838346610, ISBN-13: 978-3838346618</ref>. It can be readily extracted from Western red cedar (Thuja plicata) with solvent and ultrasonication<ref>Chedgy, Russell et al. ''Screening fungi tolerant to Western red cedar (Thuja plicata) extractives. Part 1. Mild extraction by ultrasonication and quantification of extractives by reverse-phase HPLC'' Holzforschung 61: 190–194, 2009, DOI: 10.1515/HF.2007.033</ref>.

==References==
{{reflist}}

[[Category:Tropones]]
[[Category:Monoterpenes]]

[[ja:ヒノキチオール]]
[[nl:Hinokitiol]]

Grandisol

2011-12-09T04:28:52Z

CheMoBot: Updating {{chembox}} (changes to watched fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'CASNo_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chem...

{{chembox
| Watchedfields = changed
| verifiedrevid = 450502843
| Reference=<ref name="Merck">''[[Merck Index]]'', 11th Edition, '''4442'''</ref><ref name="Science">''Science. '''1969''', ''vol. 166'' pp.1010-1012</ref>
| Name = Grandisol
| ImageFile = Grandisol.png
| ImageSize = 120px
| ImageName =
| IUPACName =(+)-(1''R'',2''S'')-1-(2'-Hydroxyethyl)-1-methyl- 2-isopropenylcyclobutane
| OtherNames =''cis''-2-Isopropenyl-1-methylcyclobutaneethanol
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 147990
| PubChem = 169202
| InChI = 1/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| InChIKey = SJKPJXGGNKMRPD-VHSXEESVBS
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = SJKPJXGGNKMRPD-VHSXEESVSA-N
| CASNo_Ref = {{cascite|correct|??}}
| CASNo = 28117-21-7
| SMILES = OCC[C@]1(C)[C@H](C(=C)C)CC1
}}
| Section2 = {{Chembox Properties
| Formula = C10H18O
| MolarMass = 154.25 g/mol
| Density =
| MeltingPt =<25 °C
| BoilingPt = 50−60 °C at 1 mmHg
}}
}}

'''Grandisol''' is a natural [[organic compound]] with the [[molecular formula]] C10H18O. It is a [[monoterpene]] containing a [[cyclobutane]] ring, an [[alcohol]] group, an [[alkene]] group and two [[Chirality (chemistry)|chiral]] centers (one of which is quaternary).

Grandisol is a [[pheromone]] primarily important as the sex attractant of the [[cotton boll weevil]] (''Anthonomus grandis''), from which it gets its name.<ref name="Merck"/> It is also a pheromone for other related insects. The cotton boll weevil is an agricultural pest that can cause significant economic damage if not controlled. Grandisol is the major constituent of the mixture known as [[grandlure]], which is used to protect cotton crops from the boll weevil.<ref name="Merck"/>

==Synthesis==
Grandisol was first isolated, identified, and synthesized by J. Tumlinson ''et al''. at Mississippi State University in 1969.<ref name="Science"/> The most recent and highest yielding synthetic route to grandisol was reported in January 2010 by a group of chemists at [[Furman University]]. <ref>{{cite journal |author=Graham, Thomas J.A.; Burgess, James M.; Gray, Erin; Goess, Brian C. |title=An Efficient Synthesis of (±)-Grandisol Featuring 1,5-Enyne Metathesis |journal=J. Org. Chem. |volume=75 |issue=1 |pages=226–228|year=2010 |month=January |pmid=19957923|pmc=2798917|doi=10.1021/jo9020375 |url=http://pubs.acs.org/doi/abs/10.1021/jo9020375}}</ref> Though enantioselective syntheses have been reported, racemic grandisol has proven equally effective at attracting boll weevils as the natural enantiomer, rendering moot the need for enantioselective syntheses for agricultural purposes.<ref>{{cite journal |author=Hibbard, B.; Webster, F. |title=Enantiomeric composition of grandisol and grandisl produced by Pissodes strobi and P. nemorensis and their electroantennogram response to pure enantiomers |journal=J. Chem. Ecol. |volume=19 |issue=10 |pages=2129–2141|year=1993 |month=October |pmid=|pmc=|doi=10.1007/BF00979652 |url=http://www.springerlink.com/content/n666313620244460/}}</ref>

==References==
{{reflist}}

[[Category:Alcohols]]
[[Category:Pheromones]]
[[Category:Alkenes]]

[[hu:Grandizol]]

Triphenylmethylradikal

2011-11-25T19:38:09Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'CASNo_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chemicals|er...

{{Chembox
| verifiedrevid = 462238281
| ImageFile = Triphenylmethylradical.png
| ImageFile_Ref = {{chemboximage|correct|??}}
| ImageName = Kekulé, skeletal formula of the triphenylmethyl radical
| Section1 = {{Chembox Identifiers
| ChemSpiderID = 10627185
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| SMILES = c1ccc(cc1)[C](c1ccccc1)c1ccccc1
| SMILES1 = C1=CC=C(C=C1)[C](C1=CC=CC=C1)C1=CC=CC=C1
| StdInChI = 1S/C19H15/c1-4-10-16(11-5-1)19(17-12-6-2-7-13-17)18-14-8-3-9-15-18/h1-15H
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = OHSJPLSEQNCRLW-UHFFFAOYSA-N
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
}}
| Section2 = {{Chembox Properties
| C = 19
| H = 15
| ExactMass = 243.117375480 g mol-1
}}
}}

The '''triphenylmethyl radical''' is a [[persistent radical]] and the first-ever [[radical (chemistry)|radical]] described in [[organic chemistry]]. It can be prepared by [[homolysis]] of [[triphenylmethyl chloride]] '''1''' (''scheme 1'') by a metal like [[silver]] or [[zinc]] in [[benzene]] or [[diethyl ether]]. The radical '''2''' forms a [[chemical equilibrium]] with the [[quinoid]] type [[Dimer (chemistry)|dimer]] '''3'''. In benzene the concentration of the radical is 2% <ref>''Advanced Organic Chemistry'' J. March, John Wiley & Sons ISBN 0-471-88841-9</ref>.

[[Image:TriphenylmethylRadical.png|400px|center|Scheme 1 Triphenylmethyl radical]]

Solutions containing the radical are [[yellow]] and when the temperature of the solution is increased the yellow color becomes more intense as the equilibrium is shifted in favor of the radical following [[Le Chatelier's principle]]. Conversely when the solution is cooled it becomes less yellow.

When exposed to air the radical rapidly oxidizes to the [[peroxide]] (''Scheme 2'') and the color of the solution changes from yellow to colorless. Likewise, the radical reacts with [[iodine]] to triphenylmethyl iodide.

[[Image:Triphenylmethyl radical oxidation.png|300px|center|Scheme 2 Triphenylmethyl radical oxidation]]

The radical was discovered by [[Moses Gomberg]] in 1900.<ref>{{cite journal | title = An instance of trivalent carbon: triphenylmethyl | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1900 | volume = 22 | issue = 11 | pages = 757–771 | doi = 10.1021/ja02049a006}}</ref><ref>{{cite journal | title = On trivalent carbon | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1901 | volume = 23 | issue = 7 | pages = 496–502 | doi = 10.1021/ja02033a015}} (Note: radical is also called a ''cadicle'')</ref><ref>{{cite journal | title = On trivalent carbon | author = [[Moses Gomberg|M. Gomberg]] | journal = [[J. Am. Chem. Soc.]] | year = 1902 | volume = 24 | issue = 7 | pages = 597–628 | doi = 10.1021/ja02021a001}}</ref> He tried to prepare hexaphenylethane from [[triphenylmethyl chloride]] and [[zinc]] in [[benzene]] in a [[Wurtz reaction]] and found that the product, based on its behaviour towards iodine and oxygen, was far more reactive than anticipated.

The correct quinoid structure for the dimer was suggested as early as 1904 but this structure was soon after abandoned by the scientific community in favor of [[hexaphenylethane]] which is structure '''4''' in scheme 1 <ref>{{cite journal | title = The hexaphenylethane riddle | author = J. M. McBride | journal = [[Tetrahedron (journal)|Tetrahedron]] | volume = 30 | issue = 14 | year = 1974 | pages = 2009–2022 | doi = 10.1016/S0040-4020(01)97332-6}}</ref>. It subsequently took until 1968 for its rediscovery when researchers at the [[Vrije Universiteit Amsterdam]] published [[proton NMR]] data <ref>{{cite journal | title = A new interpretation of the monomer-dimer equilibrium of triphenylmethyl- and alkylsubstituted-diphenyl methyl-radicals in solution | author = H. Lankamp, W. Th. Nauta and C. MacLean | journal = [[Tetrahedron Letters]] | volume = 9 | issue = 2 |year = 1968 | pages = 249–254 | doi = 10.1016/S0040-4039(00)75598-5}}</ref>. In hindsight the substituted [[ethane]] molecule does not make sense at all because it is simply too [[steric hindrance|sterically overcrowded]].

==Miscellany==
Gomberg concluded his 1900 article with the sentence "This work will be continued and I wish to reserve the field for myself." He ended his 1901 article by writing, "It is my intention to extend this study to other oxygen compounds, as well as to nitrogen derivatives, and I beg to reserve this field for further work." It is true that nineteenth-century chemists did not intrude on each other's research; to his dismay, Gomberg found out that this was not the case in the twentieth century.

==References==
{{reflist}}

==External links==
* [[Molecule of the Month]] June 1997 [http://www.chm.bris.ac.uk/motm/triphenylmethyl/main1.html Link]
* Experimental procedures [http://www.faidherbe.org/site/cours/dupuis/triphen2.htm Link]

[[Category:Free radicals]]

[[it:Radicale trifenilmetile]]
[[ru:Трифенилметил]]
[[uk:Трифенілметил]]
[[zh:三苯甲基自由基]]

Benzo(a)fluoranthen

2011-11-12T19:20:09Z

CheMoBot: Updating {{chembox}} (changes to verified fields - added verified revid - updated 'ChemSpiderID_Ref', 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'CASNo_Ref') per [[WP:CHEMVALID|Chem/Drugbo...

{{DISPLAYTITLE:Benzo(a)fluoranthene}}
{{correct title|reason=bracket|Benzo[''a'']fluoranthene}}
{{Chembox
| Verifiedfields = changed
| verifiedrevid = 459952610
|Name = Benzo[''a'']fluoranthene
|ImageFile = Benzo a fluoranthene.png
|IUPACName=
|OtherNames=
|Section1= {{Chembox Identifiers
| InChIKey = FTOVXSOBNPWTSH-UHFFFAOYAM
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = FTOVXSOBNPWTSH-UHFFFAOYSA-N
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 8792
| InChI = 1/C20H12/c1-2-7-14-13(6-1)12-19-16-9-4-3-8-15(16)18-11-5-10-17(14)20(18)19/h1-12H
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C20H12/c1-2-7-14-13(6-1)12-19-16-9-4-3-8-15(16)18-11-5-10-17(14)20(18)19/h1-12H
| SMILES =
| MeSHName=
}}
|Section2= {{Chembox Properties
| Formula=C20H12
| MolarMass =252.3093
| Appearance= Orange-yellow needles
| Density=
| MeltingPt = 144–145 °C
| BoilingPt =
}}
|Section3= {{Chembox Hazards
| FlashPt=
}}
}}

'''Benzo[''a'']fluoranthene''' is an organic [[Chemical compound|compound]] with the [[chemical formula]] C20H12.

{{PAHs}}

[[Category:Polycyclic aromatic hydrocarbons]]

{{hydrocarbon-stub}}

Natriumthiopental

2011-10-31T09:25:52Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - added verified revid - updated '') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 458267819
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = Sodium thiopental.svg
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| Drugs.com = {{drugs.com|monograph|thiopental-sodium}}
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1–2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= }}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= }}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 9561
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|changed|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|changed|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref> It is also usually the first of three drugs administered during most [[lethal injection]]s in the United States.


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1–2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18 |author-separator=, |author2=Barceló B |author3=Homar J |display-authors=3 |last4=Abadal |first4=JM |last5=Molina |first5=FJ |last6=De La Peña |first6=A |last7=Sahuquillo |first7=J |last8=Ibáñez |first8=J}}</ref> in reducing intracranial pressure.This phenomena is also termed as Reverse steal Effect.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental is questionable.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help relieve trauma in surviving victims of the [[Holocaust]].<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
Thiopental rapidly and easily crosses the blood brain barrier as it is a lipophillic molecule. As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue, due to its very high fat:water partition coefficient (aprx 10), leading to sequestration in fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |author-separator=, |author2=Chantin C |author3=Boulieu R |display-authors=3 |last4=Cotte |first4=J |last5=Berthier |first5=JC |last6=Fraisse |first6=D |last7=Bobenrieth |first7=MJ}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |author-separator=, |author2=Gómez-Cambronero L |author3=Alberola A |display-authors=3 |last4=Fabregat |first4=G |last5=Cerdá |first5=M |last6=Escobar |first6=J |last7=Sabater |first7=L |last8=García-De-La-Asuneión |first8=J |last9=Viña |first9=J}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
[[de:Thiopental]]
[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

1-Methylimidazol

2011-10-25T12:27:04Z

CheMoBot: Updating {{chembox}} (changes to verified fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors or [[user talk:CheMoBot|...

{{chembox
| Verifiedfields = changed
| verifiedrevid = 457305897
| Name = '''1-Methylimidazole'''
| ImageFile= MeIm_main.png
| ImageSize= 100px
| IUPACName = 1-Methylimidazole
| OtherNames = N-Methylimidazole
| Section1 = {{Chembox Identifiers
| SMILES = n1ccn(c1)C
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 113454
| ChemSpiderID = 1348
| InChIKey = MCTWTZJPVLRJOU-UHFFFAOYAU
| SMILES1 = Cn1ccnc1
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 543
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = MCTWTZJPVLRJOU-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 616-47-7
| RTECS =
| InChI = 1/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
}}
| Section2 = {{Chembox Properties
| Formula = C4H6N2
| MolarMass = 82.10 g/mol
| Density = 1.03 g/cm³
| MeltingPt = -60 °C
| BoilingPt = 198 °C
| pKa =
}}
| Section7 = {{Chembox Hazards
| EUClass = Harmful (Xn); Corrosive (C)
| ExternalMSDS = [http://msds.chem.ox.ac.uk/ME/1-methylimidazole.html Oxford MSDS] }}
}}

'''1-Methylimidazole''' or '''N-Methylimidazole''' is an [[aromatic]] [[heterocyclic]] organic compound with the formula CH3C3H3N2. Its N-methylation removes the possibility of tautomerization, which occurs in [[imidazole]] and many imidazole derivatives. 1-Methylimidazole maintains the pyridine-like nitrogen of imidazole, only with a slightly higher pKa.<ref>Albert, A., Heterocyclic Chemistry, 2nd ed.; 1968 Athlone Press, ISBN 048511092X</ref> The methylation also provides a significantly lower melting point, which makes 1-methylimidazole a useful solvent.

1-Methylimidazole has found use as a solvent, a base, a catalyst, a mimic for purine nucleoside bases and histidine and histamine, and as an ionic liquid precursor.

[[Image:MeIm pKa.png|500px]]

==Synthesis==

1-Methylimidazole is synthesized on an industrial scale by the [[Debus-Radziszewski imidazole synthesis|Radziszewski reaction]] from [[glyoxal]], [[formaldehyde]], and a mixture of [[ammonia]] and [[methylamine]].<ref name=Ebel>Ebel, K., Koehler, H., Gamer, A. O., & Jäckh, R. “Imidazole and Derivatives.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2002 Wiley-VCH, {{DOI|10.1002/14356007.a13_661}}</ref><ref>{{cite journal
| title = Ueber die Constitution des Lophins und verwandter Verbindungen
| author = Bronislas Radziszewski
| journal = [[Berichte der deutschen chemischen Gesellschaft]]
| volume = 15
| issue = 2
| pages = 1493–1496
| year = 1882
| url =
| doi = 10.1002/cber.18820150207 }}</ref>

:[[Image:MeIm Rad rxn.png|500px]]

The compound can also be synthesized on a laboratory scale by [[methylation]] of imidazole at the [[pyridine]]-like nitrogen and subsequent deprotonation.<ref>Gilchrist, T. L., Heterocyclic Chemistry, 2nd ed.; 1992 Longman Scientific & Technical, ISBN 0-582-06420-1</ref> Similarly, 1-methylimidazole may be synthesized by first deprotonating imidazole to form a sodium salt followed by methylation.<ref>Grimmett, M. R., Imidazole and Benzimidazole Synthesis; 1997 Academic Press, ISBN 0-12-303190-7</ref><ref>Gupta, R. R., Kumar, M., Gupta, V., Heterocyclic Chemistry II: Five Membered Heterocycles; 1999 Springer, ISBN 3-540-65252-3</ref>

:[[Image:MeIm me rxn.png|500px]]

==Biomolecule analog==
The imidazole backbone is an essential functional unit in biology. The amino acid histidine, the signaling molecule histamine, and the purine nucleobases all contain an imidazole ring.<ref name=Ebel/>

[[Image:MeIm bio.png|500px]]

1-Methylimidazole and its derivatives have been used to mimic aspects of these biomolecules. These mimics can be useful in studies to elucidate biological mechanisms and as portions of synthetic bioactive molecules.

1-Methylimidazole is also the precursor for the synthesis of the methylimidazole monomer of pyrrole-imidazole polyamides. These polymers can selectively bind specific sequences of double-stranded DNA by intercalating in a sequence dependent manner.<ref>Baird, E.E. & Dervan, P.B. J. Am. Chem. Soc. 118 (26), 6141-6146, 1996.</ref>

==Ionic liquid precursor==
1-Methylimidazole alkylates to form dialkyl imidazolium salts. Depending on the alkylating agent and the counteranion, various [[ionic liquid]]s result, e.g. [[1-butyl-3-methylimidazolium hexafluorophosphate]] ("BMIMPF6"):<ref name=Meindersma>Meindersma, W., Maase, M., and De Haan, A. B. “Ionic Liquids.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2007 Wiley-VCH, {{DOI|10.1002/14356007.l14_l01}}</ref><ref>{{OrgSynth | author = Dupont, J., Consorti, C., Suarez, P., de Souza, R. | title = Preparation of 1-Butyl-3-methyl imidazolium-based Room Temperature Ionic Liquids | collvol = 10 | collvolpages = 184 | year = 2004 | prep = v79p0236}}</ref>

:[[Image:MeIm IL.png|500px]]

BASF has used 1-methylimidazole as a means to remove acid during their industrial-scale production of diethoxyphenylphosphine. In this biphasic acid scavenging using ionic liquids (BASIL) process, 1-methylimidazole reacts with HCl to produce 1-methylimidazolium chloride, a salt that is easily separated and deprotonated to regenerate 1-methylimidazole.<ref name=Meindersma/>
:2 MeC3N2H3 + C6H5PCl2 + 2 C2H5OH → 2 [MeC3N2H4]Cl + C6H5P(OC2H5)2

==References==
{{reflist}}

{{DEFAULTSORT:Methylimidazole, 1-}}
[[Category:Imidazoles]]

Natriumthiopental

2011-10-23T12:29:14Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated 'CAS_number_Ref') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| Drugs.com = {{drugs.com|monograph|thiopental-sodium}}
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1–2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= }}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= }}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 9561
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref> It is also usually the first of three drugs administered during most [[lethal injection]]s in the United States.


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1–2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18 |author-separator=, |author2=Barceló B |author3=Homar J |display-authors=3 |last4=Abadal |first4=JM |last5=Molina |first5=FJ |last6=De La Peña |first6=A |last7=Sahuquillo |first7=J |last8=Ibáñez |first8=J}}</ref> in reducing intracranial pressure.This phenomena is also termed as Reverse steal Effect.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental is questionable.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help relieve trauma in surviving victims of the [[Holocaust]].<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
Thiopental rapidly and easily crosses the blood brain barrier as it is a lipophillic molecule. As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue, due to its very high fat:water partition coefficient (aprx 10), leading to sequestration in fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |author-separator=, |author2=Chantin C |author3=Boulieu R |display-authors=3 |last4=Cotte |first4=J |last5=Berthier |first5=JC |last6=Fraisse |first6=D |last7=Bobenrieth |first7=MJ}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |author-separator=, |author2=Gómez-Cambronero L |author3=Alberola A |display-authors=3 |last4=Fabregat |first4=G |last5=Cerdá |first5=M |last6=Escobar |first6=J |last7=Sabater |first7=L |last8=García-De-La-Asuneión |first8=J |last9=Viña |first9=J}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
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Eu(fod)3

2011-10-19T04:16:54Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'ChemSpiderID_Ref', 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref') per Chem/Drugbox validation (report...

{{chembox
| verifiedrevid = 430379155
| Name = Eufod
| ImageFile = Eufod.png
| OtherNames = Eu(fod)3
| Section1 = {{Chembox Identifiers
| CASNo = 17631-68-4
}}
| Section2 = {{Chembox Properties
| Formula = C30H30EuF21O6
| MolarMass = 1037.49 g/mol
| Appearance = Yellow powder
| Density =
| Solubility =
| MeltingPt = 203-207 °C
| BoilingPt =
}}
}}

'''Eu(fod)''' is the [[chemical compound]] with the formula Eu(OCC(CH3)3CHCOC3F7)3, also called Eu(fod)3. This [[coordination compound]] is used primarily as a shift reagent in [[NMR spectroscopy]]. It is the premier member of the [[lanthanide]] shift reagents and was popular in the 1970s and 1980s.

==Structure and reactivity==
Eu(fod)3 consists of three bidentate [[acac|acetylacetonato]] ligands bound to a [[Europium|Eu]](III) center. This metal atom has an [[electron configuration]] of f6. The six electrons are unpaired—each in a different singly-occupied [[f-orbital]]—which makes the molecule highly [[paramagnetic]]. The complex is a [[Lewis acid]], being capable of expanding its coordination number of six to eight. The complex displays a particular affinity for "[[HSAB theory|hard]]" Lewis bases, such as the oxygen atom in [[ether]]s and the nitrogen of [[amine]]s. It is soluble in nonpolar solvents, even more so than related complexes of [[acetylacetone]] and [[hexafluoroacetylacetone]]. The fod ligand is a derivative of [[heptafluorobutyric acid]].

==Uses==
===As an NMR shift reagent===
The original application of Eu(fod)3 was for analyzing diastereomeric compounds in NMR spectroscopy. The [[paramagnetic]] compound induces additional [[chemical shift]] in the protons near any Lewis basic site to which it binds in a molecule. This change helps resolve closely spaced signals by separating the ones from these hydrogens away from others that are not near basic sites but whose normal chemical shift is similar. Only small amounts of shift reagents are used, because otherwise the paramagnetism of the reagent shortens the spin-lattice relaxation times of the [[Atomic nucleus|nuclei]], which causes uncertainty broadening and loss of resolution. The availability of higher magnetic field [[spectrometers]] have lowered the demand for NMR shift reagents.

The original shift reagent was Eu(DPM)3, developed by Hinckley.<ref>C. C. Hinckley. "Paramagnetic Shifts in Solutions of Cholesterol and the Dipyridine Adduct of Trisdipivalomethanatoeuropium(III). A Shift Reagent" ''[[J. Am. Chem. Soc.]]'' 1969, volume 91, pp. 5160–5162.{{DOI|10.1021/ja01046a038}}. See also''Nature'', 1972, '''240''', 385-390</ref> Its structure is similar to Eufod, but with [[tert-butyl|''tert''-butyl]] groups in place of heptafluoropropyl substituents. That is, DPM- is the [[conjugate base]] derived from dipivaloylmethane, also known as 2,2,6,6-tetramethylheptane-3,5-dione. The ligand fod- is more lipophilic and by virtue of the perfluoralkyl substituent, its complexes are more Lewis acidic than those derived from DPM-.

===As a Lewis acid===
Eu(fod)3 serves as a Lewis acid [[catalysis|catalyst]] in organic synthesis including [[stereoselective]][[Diels-Alder]] and [[aldol]] additions. For example, Eu(fod)3 catalyzes the cyclocondensations of substituted [[dienes]] with [[aromatic]] and [[aliphatic]] [[aldehydes]] to yield dihydropyrans, with high selectivity for the [[endo]] product.<ref>Wenzel, T.J.; Ciak, J.M.; "Europium, tris(6,6,7,7,8,8,8-heptafluoro-2,2-dimethyl-3,5-octanedianato)" in ''Encyclopedia of Reagents for Organic Synthesis'', 2004. John Wiley & Sons, Ltd. {{DOI|10.1002/047084289X.rn00449}}</ref>

==References==
<references/>
{{Europium compounds}}
[[Category:Coordination compounds]]
[[Category:Acetylacetonate complexes]]
[[Category:Europium compounds]]

Natriumthiopental

2011-10-17T02:38:14Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated '') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| Drugs.com = {{drugs.com|monograph|thiopental-sodium}}
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1–2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= }}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= }}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 9561
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref> It is also usually the first of three drugs administered during most [[lethal injection]]s in the United States.


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1–2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18 |author-separator=, |author2=Barceló B |author3=Homar J |display-authors=3 |last4=Abadal |first4=JM |last5=Molina |first5=FJ |last6=De La Peña |first6=A |last7=Sahuquillo |first7=J |last8=Ibáñez |first8=J}}</ref> in reducing intracranial pressure.This phenomena is also termed as Reverse steal Effect.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental is questionable.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help relieve trauma in surviving victims of the [[Holocaust]].<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
Thiopental rapidly and easily crosses the blood brain barrier as it is a lipophillic molecule. As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue, due to its very high fat:water partition coefficient (aprx 10), leading to sequestration in fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |author-separator=, |author2=Chantin C |author3=Boulieu R |display-authors=3 |last4=Cotte |first4=J |last5=Berthier |first5=JC |last6=Fraisse |first6=D |last7=Bobenrieth |first7=MJ}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |author-separator=, |author2=Gómez-Cambronero L |author3=Alberola A |display-authors=3 |last4=Fabregat |first4=G |last5=Cerdá |first5=M |last6=Escobar |first6=J |last7=Sabater |first7=L |last8=García-De-La-Asuneión |first8=J |last9=Viña |first9=J}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
[[de:Thiopental]]
[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Grandisol

2011-09-14T17:50:25Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEMBL_Ref', 'ChEBI_Ref', 'KEGG_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chemicals|error

{{chembox
| verifiedrevid = 421073479
| Reference=<ref name="Merck">''[[Merck Index]]'', 11th Edition, '''4442'''</ref><ref name="Science">''Science. '''1969''', ''vol. 166'' pp.1010-1012</ref>
| Name = Grandisol
| ImageFile = Grandisol.png
| ImageSize = 120px
| ImageName =
| IUPACName =(+)-(1''R'',2''S'')-1-(2'-Hydroxyethyl)-1-methyl- 2-isopropenylcyclobutane
| OtherNames =''cis''-2-Isopropenyl-1-methylcyclobutaneethanol
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 147990
| PubChem = 169202
| InChI = 1/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| InChIKey = SJKPJXGGNKMRPD-VHSXEESVBS
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = SJKPJXGGNKMRPD-VHSXEESVSA-N
| CASNo = 28117-21-7
| SMILES = OCC[C@]1(C)[C@H](C(=C)C)CC1
}}
| Section2 = {{Chembox Properties
| Formula = C10H18O
| MolarMass = 154.25 g/mol
| Density =
| MeltingPt =<25 °C
| BoilingPt = 50-60 °C at 1 mmHg
}}
}}

'''Grandisol''' is a natural [[organic compound]] with the [[molecular formula]] C10H18O. It is a [[monoterpene]] containing a [[cyclobutane]] ring, an [[alcohol]] group, an [[alkene]] group and two [[Chirality (chemistry)|chiral]] centers (one of which is quaternary).

Grandisol is a [[pheromone]] primarily important as the sex attractant of the [[cotton boll weevil]] (''Anthonomus grandis''), from which it gets its name.<ref name="Merck"/> It is also a pheromone for other related insects. The cotton boll weevil is an agricultural pest that can cause significant economic damage if not controlled. Grandisol is the major constituent of the mixture known as [[grandlure]], which is used to protect cotton crops from the boll weevil.<ref name="Merck"/>

==Synthesis==
Grandisol was first isolated, identified, and synthesized by J. Tumlinson ''et al''. at Mississippi State University in 1969.<ref name="Science"/> The most recent and highest yielding synthetic route to grandisol was reported in January 2010 by a group of chemists at [[Furman University]]. <ref>{{cite journal |author=Graham, Thomas J.A.; Burgess, James M.; Gray, Erin; Goess, Brian C. |title=An Efficient Synthesis of (±)-Grandisol Featuring 1,5-Enyne Metathesis |journal=J. Org. Chem. |volume=75 |issue=1 |pages=226–228|year=2010 |month=January |pmid=19957923|pmc=2798917|doi=10.1021/jo9020375 |url=http://pubs.acs.org/doi/abs/10.1021/jo9020375}}</ref> Though enantioselective syntheses have been reported, racemic grandisol has proven equally effective at attracting boll weevils as the natural enantiomer, rendering moot the need for enantioselective syntheses for agricultural purposes.<ref>{{cite journal |author=Hibbard, B.; Webster, F. |title=Enantiomeric composition of grandisol and grandisl produced by Pissodes strobi and P. nemorensis and their electroantennogram response to pure enantiomers |journal=J. Chem. Ecol. |volume=19 |issue=10 |pages=2129–2141|year=1993 |month=October |pmid=|pmc=|doi=10.1007/BF00979652 |url=http://www.springerlink.com/content/n666313620244460/}}</ref>

==References==
{{reflist}}

[[Category:Alcohols]]
[[Category:Pheromones]]
[[Category:Alkenes]]

[[hu:Grandizol]]

Natriumthiopental

2011-08-10T18:54:22Z

CheMoBot: Updating {{drugbox}} (changes to verified and watched fields - updated 'ChEBI_Ref') per Chem/Drugbox validation (report errors or [[user talk:CheMoBot|

{{drugbox | Verifiedfields = changed
| Watchedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| ChEBI_Ref = {{ebicite|changed|EBI}}
| ChEBI = 9561
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1-2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental are dubious.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
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[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Natriumthiopental

2011-08-07T04:12:31Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated 'DrugBank_Ref', 'ChEBI_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report errors or [[us

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1-2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental are dubious.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
[[de:Thiopental]]
[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Benzamidin

2011-08-06T22:30:09Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEBI_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chemicals|errors

{{Unreferenced stub|auto=yes|date=December 2009}}
{{Chembox
| verifiedrevid = 443415204
| ImageFile = Benzamidine.svg| ImageSize = 160px
| ImageName = Skeletal formula
| ImageFile1 = Benzamidine-3D-balls.png
| ImageSize1 = 160px
| ImageName1 = Ball-and-stick model
| IUPACName=Benzenecarboximidamide
| OtherNames=
|Section1={{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2242
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = C01784
| InChI = 1/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| InChIKey = PXXJHWLDUBFPOL-UHFFFAOYAU
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 20936
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = PXXJHWLDUBFPOL-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo=618-39-3
| PubChem=2332
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 41033
| SMILES = [N@H]=C(N)c1ccccc1
}}
|Section2={{Chembox Properties
| Formula=C7H8N2
| MolarMass=120.15 g/mol
| Appearance=
| Density=
| MeltingPt=
| BoilingPt=
| Solubility=
}}
|Section3={{Chembox Hazards
| MainHazards=
| FlashPt=
| Autoignition=
}}
}}

'''Benzamidine''' is a reversible [[competitive inhibition|competitive inhibitor]] of [[trypsin]], trypsin-like enzymes and serine proteases. As a general inhibitor it can be used at 1 mM. It is sensitive to oxidation and should be prepared fresh in deionized water up to 50 mg/ml (heating may be necessary for solubilization).

It is often used as a [[ligand]] in [[protein crystallography]] to prevent [[proteases]] from degrading a protein of interest; the triangular diamine group at the bottom gives it a very obvious 'stick-man' shape which shows up in [[difference density map]]s.

[[Category:Aromatic compounds]]
[[Category:Amidines]]

{{Organic-compound-stub}}

1-Methylimidazol

2011-08-05T22:50:45Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'DrugBank_Ref', 'UNII_Ref', 'ChEBI_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject_Chem

{{chembox
| verifiedrevid = 443256367
| Name = '''1-Methylimidazole'''
| ImageFile= MeIm_main.png
| ImageSize= 100px
| IUPACName = 1-Methylimidazole
| OtherNames = N-Methylimidazole
| Section1 = {{Chembox Identifiers
| SMILES = n1ccn(c1)C
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEBI = 113454
| ChemSpiderID = 1348
| InChIKey = MCTWTZJPVLRJOU-UHFFFAOYAU
| SMILES1 = Cn1ccnc1
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 543
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = MCTWTZJPVLRJOU-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 616-47-7
| RTECS =
| InChI = 1/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
}}
| Section2 = {{Chembox Properties
| Formula = C4H6N2
| MolarMass = 82.10 g/mol
| Density = 1.03 g/cm³
| MeltingPt = -60 °C
| BoilingPt = 198 °C
| pKa =
}}
| Section7 = {{Chembox Hazards
| EUClass = Harmful (Xn); Corrosive (C)
| ExternalMSDS = [http://msds.chem.ox.ac.uk/ME/1-methylimidazole.html Oxford MSDS] }}
}}

'''1-Methylimidazole''' is an [[aromatic]] [[heterocyclic]] organic compound with the formula CH3C3H3N2. Its N-methylation removes the possibility of tautomerization, which occurs in [[imidazole]] and many imidazole derivatives. 1-Methylimidazole maintains the pyridine-like nitrogen of imidazole, only with a slightly higher pKa.<ref>Albert, A., Heterocyclic Chemistry, 2nd ed.; 1968 Athlone Press, ISBN 048511092X</ref> The methylation also provides a significantly lower melting point, which makes 1-methylimidazole a useful solvent.

1-Methylimidazole has found use as a solvent, a base, a catalyst, a mimic for purine nucleoside bases and histidine and histamine, and as an ionic liquid precursor.

[[Image:MeIm pKa.png|500px]]

==Synthesis==

1-Methylimidazole is synthesized on an industrial scale by the [[Debus-Radziszewski imidazole synthesis|Radziszewski reaction]] from [[glyoxal]], [[formaldehyde]], and a mixture of [[ammonia]] and [[methylamine]].<ref name=Ebel>Ebel, K., Koehler, H., Gamer, A. O., & Jäckh, R. “Imidazole and Derivatives.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2002 Wiley-VCH, {{DOI|10.1002/14356007.a13_661}}</ref><ref>{{cite journal
| title = Ueber die Constitution des Lophins und verwandter Verbindungen
| author = Bronislas Radziszewski
| journal = [[Berichte der deutschen chemischen Gesellschaft]]
| volume = 15
| issue = 2
| pages = 1493–1496
| year = 1882
| url =
| doi = 10.1002/cber.18820150207 }}</ref>

:[[Image:MeIm Rad rxn.png|500px]]

The compound can also be synthesized on a laboratory scale by [[methylation]] of imidazole at the [[pyridine]]-like nitrogen and subsequent deprotonation.<ref>Gilchrist, T. L., Heterocyclic Chemistry, 2nd ed.; 1992 Longman Scientific & Technical, ISBN 0-582-06420-1</ref> Similarly, 1-methylimidazole may be synthesized by first deprotonating imidazole to form a sodium salt followed by methylation.<ref>Grimmett, M. R., Imidazole and Benzimidazole Synthesis; 1997 Academic Press, ISBN 0-12-303190-7</ref><ref>Gupta, R. R., Kumar, M., Gupta, V., Heterocyclic Chemistry II: Five Membered Heterocycles; 1999 Springer, ISBN 3-540-65252-3</ref>

:[[Image:MeIm me rxn.png|500px]]

==Biomolecule analog==
The imidazole backbone is an essential functional unit in biology. The amino acid histidine, the signaling molecule histamine, and the purine nucleobases all contain an imidazole ring.<ref name=Ebel/>

[[Image:MeIm bio.png|500px]]

1-Methylimidazole and its derivatives have been used to mimic aspects of these biomolecules. These mimics can be useful in studies to elucidate biological mechanisms and as portions of synthetic bioactive molecules.

1-Methylimidazole is also the precursor for the synthesis of the methylimidazole monomer of pyrrole-imidazole polyamides. These polymers can selectively bind specific sequences of double-stranded DNA by intercalating in a sequence dependent manner.<ref>Baird, E.E. & Dervan, P.B. J. Am. Chem. Soc. 118 (26), 6141-6146, 1996.</ref>

==Ionic liquid precursor==
1-Methylimidazole alkylates to form dialkyl imidazolium salts. Depending on the alkylating agent and the counteranion, various [[ionic liquid]]s result, e.g. [[1-butyl-3-methylimidazolium hexafluorophosphate]] ("BMIMPF6"):<ref name=Meindersma>Meindersma, W., Maase, M., and De Haan, A. B. “Ionic Liquids.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2007 Wiley-VCH, {{DOI|10.1002/14356007.l14_l01}}</ref><ref>{{OrgSynth | author = Dupont, J., Consorti, C., Suarez, P., de Souza, R. | title = Preparation of 1-Butyl-3-methyl imidazolium-based Room Temperature Ionic Liquids | collvol = 10 | collvolpages = 184 | year = 2004 | prep = v79p0236}}</ref>

:[[Image:MeIm IL.png|500px]]

BASF has used 1-methylimidazole as a means to remove acid during their industrial-scale production of diethoxyphenylphosphine. In this biphasic acid scavenging using ionic liquids (BASIL) process, 1-methylimidazole reacts with HCl to produce 1-methylimidazolium chloride, a salt that is easily separated and deprotonated to regenerate 1-methylimidazole.<ref name=Meindersma/>
:2 MeC3N2H3 + C6H5PCl2 + 2 C2H5OH → 2 [MeC3N2H4]Cl + C6H5P(OC2H5)2

==References==
{{reflist}}

{{DEFAULTSORT:Methylimidazole, 1-}}
[[Category:Imidazoles]]

Natriumthiopental

2011-07-31T23:18:59Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated '') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1-2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental are dubious.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
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[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
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[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Natriumthiopental

2011-07-31T21:46:46Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated 'UNII_Ref') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| width = 113
| alt = 1:1 mixture (racemate)
| image2 = Sodium-thiopental-3D-vdW-2.png


| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous


| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =


| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_number = 71-73-8
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = DB00599
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| UNII_Ref = {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738


| C=11 | H=17 | N=2 | Na=1 | O=2 | S=1
| molecular_weight = 264.32 g/mol
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|changed|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | issue = 1-2 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing skeletal muscle relaxant is given, such as 20 mg [[pancuronium bromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given to ensure rapid loss of consciousness. Although death usually occurs within ten minutes of the beginning of the injection process, some have been known to take longer.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental in execution protocols was challenged in court after a study in the medical journal ''[[The Lancet]]'' reported autopsies of executed inmates showed the level of thiopental in their bloodstream was insufficient to cause unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. Death was pronounced at 11:47 a.m., about ten minutes after the single-dose injection was administered. Including the time required to insert the IV lines and prepare the inmate, the entire process lasted 43 minutes.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead eight minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner (criminal)|William Garner]] was executed in Ohio with sodium thiopental.<ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure."<ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier.<ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

States such as Nebraska and South Dakota have turned to an Indian supplier of the drug but this move has been criticized on the grounds the chemical may deteriorate in transit to the United States.<ref>{{cite news | url = http://timesofindia.indiatimes.com/city/mumbai/US-death-row-injection-comes-from-Mumbai-firm/articleshow/7870059.cms | title = US death row injection comes from Mumbai firm | date = 5 April 2011 | work = [[Times of India]] | first=Hemali |last=Chhapia}}</ref>

A request from [[Gary Locke]] to export thiopental for lethal injections was denied by the German government.<ref>{{cite news | url =http://www.pharmazeutische-zeitung.de/index.php?id=38197 | publisher = Pharmazeutische Zeitung.de| title = Thiopental: Rösler sagt nein zu Export nach USA| date = 8 June 2011 }}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make them more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental are dubious.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 12| pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=Asa Newsletter|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF|isbn=0824065255}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==Chemistry==
Thiopental, 5-ethyl-5-(1-methylbutyl)2-thiobarbituric acid, is synthesized by the alkylation of ethylmalonic ester with 2-bromopentane in the presence of [[sodium ethoxide]]. The product ethyl-(1-methylbutyl)malonic ester undergoes heterocyclization with [[thiourea]], using sodium ethoxide as a base. It can be seen that the structure of thiopental is synonymous with [[pentobarbital]].
[[File:Sodium thiopental synthesis.png|600px|center]]
*E.H. Volwlier, D.L. Tabern, {{US Patent|2153729}} (1939).
*G.H. Donaldson, W. Bay, {{US Patent|2876225}} (1959).

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]



[[ar:بنتوثال الصوديوم]]
[[ca:Tiopental]]
[[cs:Thiopental sodný]]
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[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Phenylazid

2011-07-28T20:54:15Z

CheMoBot: Updating {{chembox}} (changes to watched fields - updated 'UNII_Ref', 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report [[Wikipe

{{chembox
| Watchedfields = changed
| verifiedrevid = 411095002
| Name = Phenyl azide
| ImageFileL1 = Phenyl-azide-A-2D-skeletal.png
| ImageSizeL1 = 100px
| ImageNameL1 = Skeletal formula
| ImageFileR1 = Phenyl-azide-3D-balls.png
| ImageNameR1 = Ball-and-stick model
| ImageSizeR1 = 125px
| IUPACName = Phenyl azide
| OtherNames = Azidobenzene
| Section1 = {{Chembox Identifiers
| SMILES = [N-]=[N+]=NC1=CC=CC=C1
| CASNo = 622-37-7
| RTECS =
}}
| Section2 = {{Chembox Properties
| C=6|H=5|N=3
| Appearance = Pale yellow, oily liquid
| Density =
| Solubility = not appreciable
| MeltingPt =
| BoilingPt = 49–50 °C at 5 mmHg
| Viscosity =
}}
| Section7 = {{Chembox Hazards
| ExternalMSDS =
| MainHazards = explosive
| FlashPt =
| RPhrases =
| SPhrases =
}}
| Section8 = {{Chembox Related
| Function = compounds
| OtherFunctn = [[Aniline]] [[Nitrobenzene]] [[Nitrosobenzene]] [[Phenylhydrazine]] [[Phenylhydroxylamine]] [[Diazonium compound|Diazonium cation]]
}}
}}

'''Phenylazide''' is an organic compound with the formula C6H5N3. It is one of the prototypical organic azides. It has a pungent odor. The structure consists of a linear [[azide]] substituent bound to a [[phenyl]] group. The C-N=N angle is approximately 120°.

==Preparation==
Phenyl azide is prepared by the [[Diazonium compound|diazotization]] of [[phenylhydrazine]] with [[nitrous acid]]:<ref name=OrgSynth >{{OrgSynth | title = Phenyl azide | author = R. O. Lindsay and C. F. H. Allen | collvol = 3 | collvolpages = 710 | year = 1955 | prep = cv3p0710}}</ref>

:C6H5NHNH2 + HNO2 → C6H5N3 + 2 H2O

==Chemical reactions==
C6H5N3 is used to make heterocycles via cycloaddition to alkenes and especially [[Azide alkyne Huisgen cycloaddition|alkynes]], particularly those bearing electronegative substituents. It reacts with [[triphenylphosphine]] to give the Staudinger reagent C6H5NP(C6H5)3. Thermolysis induces loss of N2 to give the highly reactive phenylnitrene C6H5N.<ref>W. H. Pearson, P. S. Ramamoorthyin “Phenyl Azide” Encyclopedia of Reagents for Organic Synthesis (Ed: L. Paquette) 2004, J. Wiley & Sons, New York. DOI: 10.1002/047084289.</ref>

==Safety==
Because of the potential for explosion,<ref name=OrgSynth/> a protective [[blast shield]] is recommended during purification and handling. Distillation temperatures should be as low a possible. ''[[Organic Syntheses]]'' recommends a vacuum of 5mm Hg to give a boiling point of "66–68 °C/21 mm. with a bath temperature of 70–75 °C."<ref name=OrgSynth/> The pure substance may be stored in the dark, cold, and even then the shelf-life is only weeks.

==References==

{{reflist}}

[[Category:Aromatic compounds]]
[[Category:IARC Group 3 carcinogens]]
[[Category:Azides]]

[[nl:Fenylazide]]

Phenylazid

2011-05-12T23:23:33Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (

{{chembox
| verifiedrevid = 411095002
| Name = Phenyl azide
| ImageFile = Phenyl-azide-A-2D-skeletal.png
| ImageSize = 150px
| ImageName = Skeletal formula
| ImageFile1 = Phenyl-azide-3D-balls.png
| ImageName1 = Ball-and-stick model
| IUPACName = Phenyl azide
| OtherNames = Azidobenzene
| Section1 = {{Chembox Identifiers
| SMILES =
| CASNo = 622-37-7
| RTECS =
}}
| Section2 = {{Chembox Properties
| Formula = C6H5N3
| MolarMass = 119.14 g/mol
| Appearance = pale yellow, oily
| Density = ? g/cm3, liquid
| Solubility = not appreciable
| MeltingPt = (? K)
| BoilingPt = 49–50 °C at 5 mm Hg
| Viscosity =
}}
| Section7 = {{Chembox Hazards
| ExternalMSDS =
| MainHazards = explosive
| FlashPt =
| RPhrases =
| SPhrases =
}}
| Section8 = {{Chembox Related
| Function = compounds
| OtherFunctn = [[Aniline]] [[Nitrobenzene]] [[Nitrosobenzene]] [[Phenylhydrazine]] [[Phenylhydroxylamine]] [[Diazonium compound|Diazonium cation]]
}}
}}

Phenylazide is an organic compound with the formula C6H5N3. It is one of the prototypical organic azides. It has a pungent odor. The structure consists of a linear [[azide|N=N=N]] substituent bound to a [[phenyl]] group. The C-N=N angle is approximately 120°.

==Preparation==
Phenyl azide is prepared by the [[Diazonium compound|diazotization]] of [[phenylhydrazine]] with [[nitrous acid]]:<ref>{{OrgSynth | title = Phenyl azide | author = R. O. Lindsay and C. F. H. Allen | collvol = 3 | collvolpages = 710 | year = 1955 | prep = cv3p0710}}</ref>

:C6H5NHNH2 + HNO2 → C6H5N3 + 2 H2O

==Chemical reactions==
C6H5N3 is used to make heterocycles via cycloaddition to alkenes and especially [[Azide alkyne Huisgen cycloaddition|alkynes]], particularly those bearing electronegative substituents. It reacts with [[triphenylphosphine]] to give the Staudinger reagent C6H5NP(C6H5)3. Thermolysis induces loss of N2 to give the highly reactive phenylnitrene C6H5N.<ref>W. H. Pearson, P. S. Ramamoorthyin “Phenyl Azide” Encyclopedia of Reagents for Organic Synthesis (Ed: L. Paquette) 2004, J. Wiley & Sons, New York. DOI: 10.1002/047084289.</ref>

==Safety==
A protective [[blast shield]] is needed during purification and handling. Distillation temperatures should be as low a possible. [[Organic Syntheses]] recommends a vacuum of 5mm Hg to give a boiling point of "66–68 °C/21 mm. with a bath temperature of 70–75 °C." The pure substance may be stored in the dark, cold, and even then the shelf-life is only weeks.

==References==

{{reflist}}

[[Category:Aromatic compounds]]
[[Category:IARC Group 3 carcinogens]]
[[Category:Azides]]

[[nl:Fenylazide]]

Pentosanpolysulfat-Natrium

2011-05-12T12:22:36Z

CheMoBot: Updating {{drugbox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (

{{Drugbox| verifiedrevid = 383471350
|
|IUPAC_name =
| image = Pentosan polysulfate.svg
| width = 150px
| CAS_number=37300-21-3
| ATC_prefix=C05
| ATC_suffix=BA04
| ATC_supplemental={{ATCvet|M01|AX90}}
| PubChem=37720
| DrugBank=
| C=14 | H=26 | O=21 | S=4
| molecular_weight = 658.608
| bioavailability= ?
| metabolism = ?
| elimination_half-life=?
| excretion = urine
| pregnancy_category = B
| legal_status = ?
| routes_of_administration= [[mouth|Oral]], [[intramuscular injection|intramuscular]], [[intra-articular]], [[intraventricular]]
}}
'''Pentosan polysulfate''' (sold under the name '''Elmiron''' by [[Ortho-McNeil Pharmaceutical]], inc.) is the only oral medication approved by the U.S. FDA for the treatment of [[interstitial cystitis]], also known as painful bladder syndrome.

==Uses==
===Interstitial cystitis/painful bladder syndrome===
[[Interstitial cystitis/painful bladder syndrome]] (IC/PBS) patients struggle with symptoms of urinary frequency, urgency, pressure and/or pain, as well as nocturia (frequent urination at night), dyspareunia (painful intercourse), pain and/or discomfort while sitting in a car, while driving and/or travelling.

The origin/cause of IC/PBS is unknown though a number of theories are currently under consideration. Urine cultures are typically negative for infection, yet it is not unusual for patients to believe that they have had infections for years rather than IC/PBS, because the symptoms of an infection are nearly identical to the symptoms of IC/PBS.

Pentosan polysulfate is available as pills or directly infused into the bladder.

===Transmissible spongiform encephalopathies===

Recently pentosan polysulfate has gained attention as possibly being effective in the treatment of [[Creutzfeldt-Jakob disease]] (CJD), although there is as yet no definitive evidence for this other than results of the ongoing treatment (published) of one patient in Northern Ireland and around six other patients in mainland Britain.<ref>[http://news.bbc.co.uk/1/hi/health/4306351.stm BBC NEWS | Health | Research will now assess CJD drug]</ref>

Around 15 other patients in non-UK countries have also received this treatment in an attempt to halt or slow down CJD and related disease progression.

===Osteoarthrosis in adult dogs===

Recently PPN is being marketed as an alternative for the treatment of lameness and pain of degenerative joint disease/osteoarthrosis (non-infectious arthrosis) in the skeletally mature dog.

'''Cartrophen-Vet''' is a 100mg/ml formulation of Pentosan polysulphate that has been used in Australia since the early 1990s. It is produced by Biopharm Australia [http://www.r-biopharm.com/distributors_content.php?language=english&cid=10004&sub=1&conti=Oceania&country=Australia&].

3 mg/kg PPN is given subcutaneously every 5-7 days for 4 treatments. Subsequent single booster shots are usually given every 3-6 months. <ref>[http://www.vmd.gov.uk/espcsite/Documents/176337.DOC]</ref>

==Pharmacology==
Pentosan is believed to work by providing a protective coating to the damaged bladder wall. The critical flaw of the medication, however, is its exceptionally poor bioavailability when taken orally. Research presented late in 2005 by Alza Pharmaceuticals demonstrates that more than 94% of the medication is excreted, intact, in feces without providing any beneficial effect.<ref>Simon M, McClanahan RH, Shah JF et al. Metabolism of [3H]pentosan polysulfate sodium (PPS) in healthy human volunteers. Xenobiotica. 2005 Aug;35(8):775-84. PMID 16278190</ref> Their research found that only 6% was excreted through urine. The drug must be taken for several months for most patients to achieve some benefit.

More recently, however, pentosan polysulfate has been studied as part of a "rescue instillation" which is placed directly in the bladder and can, perhaps, provide better effectiveness. C. Lowell Parsons has presented a research study which shows a 90% effectiveness in reducing the symptoms of IC/PBS patients by using this instillation.{{Fact|date=January 2008}}

==Side effects==
Patients who have taken pentosan orally report a variety of side effects, primarily GI complaints such as diarrhea, heartburn, stomach pain. Hair loss, headache, rash, insomnia have also been reported. One concern is the potential for increased blood coagulation times with this medication. Some patients have reported that they bruise more easily. In some cases, patients are asked to stop medication before any major surgical procedures to reduce the likelihood of bleeding.

==References==

{{Reflist}}

==External links==
* [http://www.ic-network.com/guestlectures/ "Meet the IC Expert" Guest Lecture by C. Lowell Parsons, MD]
* [http://www.orthoelmiron.com/ic-faqs.html Elmiron FAQ] (For Interstitial Cystitis patients)
* {{PDF|1=[http://www.myortho360.com/myortho360/assets/elmiron/Elmiron_PI.pdf Prescribing Information]}}.

{{Vasoprotectives}}
[[Category:Drugs]]
[[Category:Urologic pelvic pain syndrome]]
[[es:Pentosano polisulfato]]

Icean

2011-04-19T10:53:18Z

{{chembox
| verifiedrevid = 383390617
| Name = Iceane
| ImageFileL1 = Iceane-3D-sticks.png
| ImageSizeL1 = 100px
| ImageFileR1 = Iceane-3D-vdW.png
| ImageSizeR1 = 100px
| IUPACName = Tetracyclo[5.3.1.12,604,9]dodecane
| OtherNames = Iceane
| Section1 = {{Chembox Identifiers
| SMILES = C1C2CC3CC1C1CC2CC3C1
| CASNo = 53283-19-5
| RTECS =
| InChI= 1/C12H18/c1-7-2-11-3-8(1)10-4-9(7)5- 12(11)6-10/h7-12H,1-6H2
}}
| Section2 = {{Chembox Properties
| Formula = C12H18
| MolarMass = 163.56 g/mol
| Appearance =
| Density =
| Solubility =
| Solvent =
| SolubleOther =
| MeltingPt =
| BoilingPt =
| Viscosity =
}}
| Section3 = {{Chembox Structure
| CrystalStruct =
| Dipole =
}}
| Section7 = {{Chembox Hazards
| ExternalMSDS =
| MainHazards =
| FlashPt =
| RPhrases =
| SPhrases =
}}
| Section8 = {{Chembox Related
| Function =
| OtherFunctn =
}}
}}

'''Iceane''' is a [[saturated hydrocarbon|saturated]] [[polycyclic compound|polycyclic]] [[hydrocarbon]] with formula C12H18. It has a [[Cage (enclosure)|cage]]-like [[molecule|molecular]] structure, whose [[carbon]] skeleton can be viewed as three fused [[cyclohexane]] rings in the "boat" [[cyclohexane conformation|conformation]]; or as two such rings in the "chair" conformation, connected by three parallel bonds.

The name "iceane" was proposed by the chemist [[Louis Fieser]] about a decade before the compound was first prepared. He was carrying out studies on the arrangement of [[water]] molecules in [[ice]], when it occurred to him that there could exist a stable hydrocarbon with the above structure.{{Fact|date=November 2009}}

==See also==
* [[Adamantane]]
* [[Twistane]]
* [[Propellane]]

==References==
{{Reflist}}

==External links==
*[http://www.rsc.org/publishing/journals/article.asp?doi=C39820000372 Royal Society of Chemistry Journal]
*[http://books.google.co.uk/books?id=U-VW1MPrX0UC&pg=PA129&lpg=PA129&dq=iceane&source=web&ots=rDYPei2_Rx&sig=utmV9O3nTJcYeyEP8DJDRHW87a0&hl=en#PPA129,M1 ''Symmetry Through the Eyes of a Chemist'', Magdolna Hargittai]
*[http://books.google.com/books?id=7kvAOwqRU0sC&pg=PA68&dq=iceane&ei=COHTR_32IJGgygTghPyABA&sig=u38TtPLJfOn1kO8X4FQ9Ph-5-KI#PPA68,M1Symmetry: ''A Basis for Synthesis Design'', Tse-Lok Ho]
*[http://books.google.co.uk/books?id=2sSMEMkarFkC&pg=PA154&lpg=PA154&dq=iceane+CAS+rn&source=web&ots=C1kQeVJ9IQ&sig=JiACJW1L595tHxO9a91NSP_lqF4&hl=en#PPA154,M1 ''Structures and Energies of Polycyclic Hydrocarbons'', Joan E. Shields]

[[Category:Cycloalkanes]]

{{Organic-compound-stub}}

[[ja:アイサン]]

Eu(fod)3

2011-04-18T18:05:51Z

{{chembox
| verifiedrevid = 398718634
| Name = Eufod
| ImageFile = Eufod.png
| OtherNames = Eu(fod)3
| Section1 = {{Chembox Identifiers
| CASNo = 17631-68-4
}}
| Section2 = {{Chembox Properties
| Formula = C30H30EuF21O6
| MolarMass = 1037.49 g/mol
| Appearance = Yellow powder
| Density =
| Solubility =
| MeltingPt = 203-207 °C
| BoilingPt =
}}
}}

'''Eu(fod)''' is the [[chemical compound]] with the formula Eu(OCC(CH3)3CHCOC3F7)3, also called Eu(fod)3. This [[coordination compound]] is used primarily as a shift reagent in [[NMR spectroscopy]]. It is the premier member of the [[lanthanide]] shift reagents and was popular in the 1970s and 1980s.

==Structure and reactivity==
Eu(fod)3 consists of three bidentate [[acac|acetylacetonato]] ligands bound to a Eu(III) center. Eu(III) has an electron configuration f6, which these six electrons occupy [[f-orbital]]s. These electrons are unpaired, which implies that each molecule is highly [[paramagnetic]]. The complex is a [[Lewis acid]], being capable of expanding its coordination number of six to eight. The complex displays a particular affinity for a "[[HSAB theory|hard]]" Lewis bases, such as [[ether]]s and [[amine]]s. It is soluble in nonpolar solvents, even more so than related complexes of [[acetylacetone]] and [[hexafluoroacetylacetone]]. The fod ligand is a derivative of [[heptafluorobutyric acid]].

==Uses==
===As an NMR shift reagent===
The original application of Eu(fod)3 was for analyzing diastereomeric compounds in NMR spectroscopy. The [[paramagnetic]] compound induces shifts in the protons near the Lewis basic site(s) of the molecule, which helps to resolve closely-spaced signals. Only small amounts of shift reagents are used, because otherwise the paramagnetism of the reagent shortens the spin-lattice relaxation times of the [[Atomic nucleus|nuclei]], which causes uncertainty broadening and loss of resolution. The availability of higher magnetic field [[spectrometers]] have lowered the demand for NMR shift reagents.

The original shift reagent was Eu(DPM)3, developed by Hinckley.<ref>C. C. Hinckley. "Paramagnetic Shifts in Solutions of Cholesterol and the Dipyridine Adduct of Trisdipivalomethanatoeuropium(III). A Shift Reagent" ''[[J. Am. Chem. Soc.]]'' 1969, volume 91, pp. 5160–5162.{{DOI|10.1021/ja01046a038}}. See also''Nature'', 1972, '''240''', 385-390</ref> Its structure is similar to Eufod, but with tert-butyl groups in place of heptafluoropropyl substituents, i.e. DPM- is the [[conjugate base]] derived from dipivaloylmethane, also known as 2,2,6,6-tetramethylheptane-3,5-dione. The ligand fod- is more lipophilic and by virtue of the perfluoralkyl substituent, its complexes are more Lewis acidic than those derived from DPM-.

===As a Lewis acid===
Eu(fod)3 serves as a Lewis acid [[catalysis|catalyst]] in organic synthesis including [[stereoselective]][[Diels-Alder]] and [[aldol]] additions. For example, Eu(fod)3 catalyzes the cyclocondensations of substituted [[dienes]] with [[aromatic]] and [[aliphatic]] [[aldehydes]] to yield dihydropyrans, with high selectivity for the [[endo]] product.<ref>Wenzel, T.J.; Ciak, J.M.; "Europium, tris(6,6,7,7,8,8,8-heptafluoro-2,2-dimethyl-3,5-octanedianato)" in ''Encyclopedia of Reagents for Organic Synthesis'', 2004. John Wiley & Sons, Ltd. {{DOI|10.1002/047084289X.rn00449}}</ref>

==References==
<references/>

[[Category:Coordination compounds]]
[[Category:Acetylacetonate complexes]]
[[Category:Europium compounds]]

Grandisol

2011-03-22T12:20:22Z

CheMoBot: Updating {{chembox}} (changes to watched fields - updated 'UNII_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors or [[user talk:

{{chembox
| Watchedfields = changed
| verifiedrevid = 400101423
| Reference=<ref name="Merck">''[[Merck Index]]'', 11th Edition, '''4442'''</ref><ref name="Science">''Science. '''1969''', ''vol. 166'' pp.1010-1012</ref>
| Name = Grandisol
| ImageFile = Grandisol.png
| ImageSize = 120px
| ImageName =
| IUPACName =(+)-(1''R'',2''S'')-1-(2'-Hydroxyethyl)-1-methyl- 2-isopropenylcyclobutane
| OtherNames =''cis''-2-Isopropenyl-1-methylcyclobutaneethanol
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 147990
| PubChem = 169202
| InChI = 1/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| InChIKey = SJKPJXGGNKMRPD-VHSXEESVBS
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H18O/c1-8(2)9-4-5-10(9,3)6-7-11/h9,11H,1,4-7H2,2-3H3/t9-,10+/m0/s1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = SJKPJXGGNKMRPD-VHSXEESVSA-N
| CASNo = 28117-21-7
| SMILES = OCC[C@]1(C)[C@H](C(=C)C)CC1
}}
| Section2 = {{Chembox Properties
| Formula = C10H18O
| MolarMass = 154.25 g/mol
| Density =
| MeltingPt =<25 °C
| BoilingPt = 50-60 °C at 1 mmHg
}}
}}

'''Grandisol''' is a natural [[organic compound]] with the [[molecular formula]] C10H18O. It is a [[monoterpene]] containing a [[cyclobutane]] ring, an [[alcohol]] group, an [[alkene]] group and two [[Chirality (chemistry)|chiral]] centers (one of which is quaternary).

Grandisol is a [[pheromone]] primarily important as the sex attractant of the [[cotton boll weevil]] (''Anthonomus grandis''), from which it gets its name.<ref name="Merck"/> It is also a pheromone for other related insects. The cotton boll weevil is an agricultural pest that can cause significant economic damage if not controlled. Grandisol is the major constituent of the mixture known as [[grandlure]], which is used to protect cotton crops from the boll weevil.<ref name="Merck"/>

==Synthesis==
Gradisol was first isolated, identified, and synthesized by J. Tumlinson ''et al''. at Mississippi State University in 1969.<ref name="Science"/> The most recent and highest yielding synthetic route to grandisol was reported in January 2010 by a group of chemists at [[Furman University]]. <ref>{{cite journal |author=Graham, Thomas J.A.; Burgess, James M.; Gray, Erin; Goess, Brian C. |title=An Efficient Synthesis of (±)-Grandisol Featuring 1,5-Enyne Metathesis |journal=J. Org. Chem. |volume=75 |issue=1 |pages=226–228|year=2010 |month=January |pmid=19957923|pmc=2798917|doi=10.1021/jo9020375 |url=http://pubs.acs.org/doi/abs/10.1021/jo9020375}}</ref> Though enantioselective syntheses have been reported, racemic grandisol has proven equally effective at attracting boll weevils as the natural enantiomer, rendering moot the need for enantioselective syntheses for agricultural purposes.<ref>{{cite journal |author=Hibbard, B.; Webster, F. |title=Enantiomeric composition of grandisol and grandisl produced by Pissodes strobi and P. nemorensis and their electroantennogram response to pure enantiomers |journal=J. Chem. Ecol. |volume=19 |issue=10 |pages=2129–2141|year=1993 |month=October |pmid=|pmc=|doi=10.1007/BF00979652 |url=http://www.springerlink.com/content/n666313620244460/}}</ref>

==References==
{{reflist}}

[[Category:Alcohols]]
[[Category:Pheromones]]
[[Category:Alkenes]]

Ethylazid

2011-03-21T23:50:51Z

{{chembox
| verifiedrevid = 411425300
| ImageFile = Ethyl azide.svg
| ImageSize =
| IUPACName =Azidoethane
| OtherNames = Ethane, azido-; 1-Azidoethane
| Section1 = {{Chembox Identifiers
| CAS No 871-31-8
| UN Number =
| PubChem =79118
| SMILES =
}}
| Section2 = {{Chembox Properties
| Formula = C2H5N3
| MolarMass = 71.08
| Appearance = liquid
| Density =
| MeltingPt =
| BoilingPt = 50
| Solubility =
| SolubleOther =
}}
| Section3 = {{Chembox Explosive
| ShockSens = High
| FrictionSens = High
| ExplosiveV =
| REFactor = }}
| Section4 = {{Chembox Thermochemistry
| DeltaHc =
| DeltaHf = 266.872
| Entropy =
| HeatCapacity = }}

| Section5 = {{Chembox Hazards
| MainHazards = Harmful, Explosive
| FlashPt =
| Autoignition = }}
| Section8 = {{Chembox Related
| OtherAnions =
| OtherCations =
| OtherFunctn =
| Function =
| OtherCpds = [[Hydrazoic acid]], [[Chlorine azide]], [[Methyl azide]] }}
}}

'''Ethyl azide''' C2H5N3 is an explosive compound sensitive to rapid heating, shock or impact. It has exploded when heated to room temperature.<ref>{{cite journal | last1 =Campbell | first1 =Hallock C. | last2 =Rice | first2 =O. K. | journal =Journal of the American Chemical Society | volume =57 | pages =1044 | year =1935 | doi =10.1021/ja01309a019}}</ref><ref>{{cite journal | last1 =Rice | first1 =O. K. | last2 =Campbell | first2 =Hallock C. | title =The Explosion of Ethyl Azide in the Presence of Diethyl Ether | journal =The Journal of Chemical Physics | volume =7 | pages =700 | year =1939 | doi =10.1063/1.1750516}}</ref> When heated to decomposition it emits toxic fumes of [[NOx]].<ref>{{cite journal | last1 =Rice | first1 =O. K. | title =The Role of Heat Conduction in Thermal Gaseous Explosions | journal =The Journal of Chemical Physics | volume =8 | pages =727 | year =1940 | doi =10.1063/1.1750808}}</ref><ref>{{cite journal | last1 =Costa Cabral | first1 =B. J. | last2 =Costa | first2 =M. L. | last3 =Almoster Ferreira | first3 =M. A. | title =ChemInform Abstract: Molecular Structure and Ionization Energies of Azides: an ab initio Study of Hydrazoic Acid, Methyl Azide and Ethyl Azide | journal =ChemInform | volume =24 | pages =no | year =2010 | doi =10.1002/chin.199337053}}</ref>

It is irritating to eyes, respiratory system and skin.

==Uses==
Ethyl azide is used in [[organic synthesis]].

==References==
{{reflist}}

[[Category:Azides]]
[[Category:Explosive chemicals]]

[[ja:アジ化エチル]]

Hinokitiol

2011-02-23T16:24:53Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report [[Wikipedia_t

{{Chembox
| verifiedrevid = 415528328
| Reference = <ref>[http://www.sigmaaldrich.com/catalog/ProductDetail.do?N4=469521|ALDRICH&N5=SEARCH_CONCAT_PNO|BRAND_KEY&F=SPEC β-Thujaplicin] at [[Sigma-Aldrich]]</ref>
| ImageFile = beta-thujaplicin.png
| ImageSize = 150px
| IUPACName = 2-Hydroxy-6-propan-2-ylcyclohepta-2,4,6-trien-1-one
| OtherNames = β-Thujaplicin; 4-Isopropyltropolone
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 3485
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = D04876
| InChI = 1/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| InChIKey = FUWUEFKEXZQKKA-UHFFFAOYAT
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 48310
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C10H12O2/c1-7(2)8-4-3-5-9(11)10(12)6-8/h3-7H,1-2H3,(H,11,12)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = FUWUEFKEXZQKKA-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 499-44-5
| PubChem = 3611
| SMILES = O=C1/C=C(\C=C/C=C1/O)C(C)C
}}
| Section2 = {{Chembox Properties
| C=10|H=12|O=2
| Appearance = Colorless to pale yellow crystals
| Density =
| MeltingPt = 50-52 °C
| BoilingPt = 140 °C at 10 mmHg
| Solubility = }}
| Section3 = {{Chembox Hazards
| MainHazards =
| FlashPt = 140 °C
| Autoignition = }}
}}

'''Hinokitiol''' ('''β-thujaplicin''') is a natural [[Terpenoid|monoterpenoid]] found in the wood of trees in the family [[Cupressaceae]]. It is a [[tropolone]] derivative and one of the [[thujaplicin]]s. Hinokitiol has inhibitory effects on ''[[Chlamydia trachomatis]]'' and may be clinically useful as a topical drug.<ref>{{cite journal | doi = 10.1128/AAC.49.6.2519-2521.2005 | url = http://aac.asm.org/cgi/content/full/49/6/2519 | pmid = 15917561 | year = 2005 | last1 = Yamano | first1 = H | last2 = Yamazaki | first2 = T | last3 = Sato | first3 = K | last4 = Shiga | first4 = S | last5 = Hagiwara | first5 = T | last6 = Ouchi | first6 = K | last7 = Kishimoto | first7 = T | title = In vitro inhibitory effects of hinokitiol on proliferation of Chlamydia trachomatis | volume = 49 | issue = 6 | pages = 2519–21 | journal = Antimicrobial agents and chemotherapy | pmc = 1140513}}</ref>

==References==
{{reflist}}

[[Category:Tropolones]]
[[Category:Monoterpenes]]

[[ja:ヒノキチオール]]
[[nl:Hinokitiol]]

Natriumthiopental

2011-02-15T02:39:57Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated 'KEGG_Ref') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| alt = 1:1 mixture (racemate)
| width = 113
| image2 = Sodium-thiopental-3D-vdW-2.png
| StdUNII_Ref = {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| ChEMBL_Ref = {{ebicite|changed|EBI}}
| ChEMBL = 738
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| InChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
| CAS_number = 71-73-8
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = DB00599
| KEGG_Ref = {{keggcite|changed|kegg}}
| KEGG = D00714
| C = 11 | H = 17 | N = 2 | Na = 1 | O = 2 | S = 1
| molecular_weight = 264.32 g/mol
| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg [[pancuronium dibromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for [[pancuronium]] dibromide (Pavulon) are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given, placing the subject into a rapidly induced coma. Executions using the three-drug combination are usually effective in approximately 10 minutes, but have been known to take several times this amount of time. The use of thiopental alone is hypothesized to cause death in approximately 45 minutes.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental has been the cause of current Supreme Court challenges to the lethal injection protocol, after a study in the medical journal ''[[The Lancet]]'', where autopsy studies on executed inmates revealed that there was not a high enough concentration of thiopental in their blood to have caused unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. The execution took 43 minutes and was concluded at 11:47 a.m., including approximately 30 minutes to complete the process of inserting the needle, and about 10 minutes between administering the single dose and the pronouncement of death.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead 8 minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner]] was executed in Ohio with sodium thiopental. <ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure." <ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier. <ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make him more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. The drug tends to make subjects chatty and cooperative with interrogators; however, the reliability of confessions made under thiopental is dubious.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 137 | pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of sodium thiopental is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=ASA NEWSLETTER|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless only 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]


[[ar:بنتوثال الصوديوم]]
[[ca:Thiopental]]
[[cs:Thiopental sodný]]
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[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

Benzamidin

2011-02-14T15:15:13Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors

{{Unreferenced stub|auto=yes|date=December 2009}}
{{Chembox
| verifiedrevid = 413885168
| ImageFile = Benzamidine.svg| ImageSize = 160px
| ImageName = Skeletal formula
| ImageFile1 = Benzamidine-3D-balls.png
| ImageSize1 = 160px
| ImageName1 = Ball-and-stick model
| IUPACName=Benzenecarboximidamide
| OtherNames=
|Section1={{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2242
| KEGG_Ref = {{keggcite|correct|kegg}}
| KEGG = C01784
| InChI = 1/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| InChIKey = PXXJHWLDUBFPOL-UHFFFAOYAU
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 20936
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C7H8N2/c8-7(9)6-4-2-1-3-5-6/h1-5H,(H3,8,9)
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = PXXJHWLDUBFPOL-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo=618-39-3
| PubChem=2332
| SMILES = [N@H]=C(N)c1ccccc1
}}
|Section2={{Chembox Properties
| Formula=C7H8N2
| MolarMass=120.15 g/mol
| Appearance=
| Density=
| MeltingPt=
| BoilingPt=
| Solubility=
}}
|Section3={{Chembox Hazards
| MainHazards=
| FlashPt=
| Autoignition=
}}
}}

'''Benzamidine''' is a reversible [[competitive inhibition|competitive inhibitor]] of [[trypsin]], trypsin-like enzymes and serine proteases. As a general inhibitor it can be used at 1 mM. It is sensitive to oxidation and should be prepared fresh in deionized water up to 50 mg/ml (heating may be necessary for solubilization).

It is often used as a [[ligand]] in [[protein crystallography]] to prevent [[proteases]] from degrading a protein of interest; the triangular diamine group at the bottom gives it a very obvious 'stick-man' shape which shows up in [[difference density map]]s.

[[Category:Aromatic compounds]]
[[Category:Amidines]]

{{Organic-compound-stub}}

1-Methylimidazol

2011-02-10T12:01:12Z

CheMoBot: Updating {{chembox}} (no changed fields - added verified revid - updated 'UNII_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors

{{chembox
| verifiedrevid = 413092634
| Name = '''1-Methylimidazole'''
| ImageFile= MeIm_main.png
| ImageSize= 100px
| IUPACName = 1-Methylimidazole
| OtherNames = N-Methylimidazole
| Section1 = {{Chembox Identifiers
| SMILES = n1ccn(c1)C
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 1348
| InChIKey = MCTWTZJPVLRJOU-UHFFFAOYAU
| SMILES1 = Cn1ccnc1
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 543
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = MCTWTZJPVLRJOU-UHFFFAOYSA-N
| CASNo_Ref = {{cascite|correct|CAS}}
| CASNo = 616-47-7
| RTECS =
| InChI = 1/C4H6N2/c1-6-3-2-5-4-6/h2-4H,1H3
}}
| Section2 = {{Chembox Properties
| Formula = C4H6N2
| MolarMass = 82.10 g/mol
| Density = 1.03 g/cm³
| MeltingPt = -60 °C
| BoilingPt = 198 °C
| pKa =
}}
| Section7 = {{Chembox Hazards
| EUClass = Harmful (Xn); Corrosive (C)
| ExternalMSDS = [http://msds.chem.ox.ac.uk/ME/1-methylimidazole.html Oxford MSDS] }}
}}

'''1-Methylimidazole''' is an [[aromatic]] [[heterocyclic]] organic compound with the formula CH3C3H3N2. Its N-methylation removes the possibility of tautomerization, which occurs in [[imidazole]] and many imidazole derivatives. 1-Methylimidazole maintains the pyridine-like nitrogen of imidazole, only with a slightly higher pKa. <ref>Albert, A., Heterocyclic Chemistry, 2nd ed.; 1968 Athlone Press, ISBN 048511092X</ref> The methylation also provides a significantly lower melting point, which makes 1-methylimidazole a useful solvent.

1-Methylimidazole has found use as a solvent, a base, a catalyst, a mimic for purine nucleoside bases and histidine and histamine, and as an ionic liquid precursor.

[[Image:MeIm pKa.png|500px]]

==Synthesis==

1-Methylimidazole is synthesized on an industrial scale by the [[Debus-Radziszewski imidazole synthesis|Radziszewski reaction]] from [[glyoxal]], [[formaldehyde]], and a mixture of [[ammonia]] and [[methylamine]]. <ref name=Ebel>Ebel, K., Koehler, H., Gamer, A. O., & Jäckh, R. “Imidazole and Derivatives.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2002 Wiley-VCH, {{DOI|10.1002/14356007.a13_661}}</ref><ref>{{cite journal
| title = Ueber die Constitution des Lophins und verwandter Verbindungen
| author = Bronislas Radziszewski
| journal = [[Berichte der deutschen chemischen Gesellschaft]]
| volume = 15
| issue = 2
| pages = 1493 – 1496
| year = 1882
| url =
| doi = 10.1002/cber.18820150207 }}</ref>

:[[Image:MeIm Rad rxn.png|500px]]

The compound can also be synthesized on a laboratory scale by [[methylation]] of imidazole at the [[pyridine]]-like nitrogen and subsequent deprotonation.<ref>Gilchrist, T. L., Heterocyclic Chemistry, 2nd ed.; 1992 Longman Scientific & Technical, ISBN 0-582-06420-1</ref> Similarly, 1-methylimidazole may be synthesized by first deprotonating imidazole to form a sodium salt followed by methylation. <ref>Grimmett, M. R., Imidazole and Benzimidazole Synthesis; 1997 Academic Press, ISBN 0-12-303190-7</ref><ref>Gupta, R. R., Kumar, M., Gupta, V., Heterocyclic Chemistry II: Five Membered Heterocycles; 1999 Springer, ISBN 3-540-65252-3</ref>

:[[Image:MeIm me rxn.png|500px]]

==Biomolecule analog==
The imidazole backbone is an essential functional unit in biology. The amino acid histidine, the signaling molecule histamine, and the purine nucleobases all contain an imidazole ring. <ref name=Ebel/>

[[Image:MeIm bio.png|500px]]

1-Methylimidazole and its derivatives have been used to mimic aspects of these biomolecules. These mimics can be useful in studies to elucidate biological mechanisms and as portions of synthetic bioactive molecules.

1-Methylimidazole is also the precursor for the synthesis of the methylimidazole monomer of pyrrole-imidazole polyamides. These polymers can selectively bind specific sequences of double-stranded DNA by intercalating in a sequence dependent manner.<ref>Baird, E.E. & Dervan, P.B. J. Am. Chem. Soc. 118 (26), 6141-6146, 1996.</ref>

==Ionic liquid precursor==
1-Methylimidazole alkylates to form dialkyl imidazolium salts. Depending on the alkylating agent and the counteranion, various [[ionic liquid]]s result, e.g. [[1-butyl-3-methylimidazolium hexafluorophosphate]] ("BMIMPF6"):<ref name=Meindersma>Meindersma, W., Maase, M., and De Haan, A. B. “Ionic Liquids.” In Ullmann’s Encyclopedia of Industrial Chemistry; 2007 Wiley-VCH, {{DOI|10.1002/14356007.l14_l01}}</ref><ref>{{OrgSynth | author = Dupont, J., Consorti, C., Suarez, P., de Souza, R. | title = Preparation of 1-Butyl-3-methyl imidazolium-based Room Temperature Ionic Liquids | collvol = 10 | collvolpages = 184 | year = 2004 | prep = v79p0236}}</ref>

:[[Image:MeIm IL.png|500px]]

BASF has used 1-methylimidazole as a means to remove acid during their industrial-scale production of diethoxyphenylphosphine. In this BASIL (Biphasic Acid Scavenging utilizing Ionic Liquids) process, 1-methylimidazole reacts with HCl to produce 1-methylimidazolium chloride, a salt that is easily separated and deprotonated to regenerate 1-methylimidazole.<ref name=Meindersma/>
:2 MeC3N2H3 + C6H5PCl2 + 2 C2H5OH → 2 [MeC3N2H4]Cl + C6H5P(OC2H5)2

==References==
{{reflist}}

{{DEFAULTSORT:Methylimidazole, 1-}}
[[Category:Imidazoles]]

Ethylazid

2011-02-01T19:07:46Z

CheMoBot: Updating {{chembox}} (changes to watched fields - added verified revid - updated 'UNII_Ref', 'ChemSpiderID_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per [[Wikipedia:WikiProject Chemicals/Chembox validation|Chem/Drugbox valida

{{chembox
| Watchedfields = changed
| verifiedrevid = 411342589
| ImageFile = Ethyl azide.svg
| ImageSize =
| IUPACName =Azidoethane
| OtherNames = Ethane, azido-; 1-Azidoethane
| Section1 = {{Chembox Identifiers
| CAS No 871-31-8
| UN Number =
| PubChem =79118
| SMILES =
}}
| Section2 = {{Chembox Properties
| Formula = C2H5N3
| MolarMass = 71.08
| Appearance = liquid
| Density =
| MeltingPt =
| BoilingPt = 50
| Solubility =
| SolubleOther =
}}
| Section3 = {{Chembox Explosive
| ShockSens = High
| FrictionSens = High
| ExplosiveV =
| REFactor = }}
| Section4 = {{Chembox Thermochemistry
| DeltaHc =
| DeltaHf = 266.872
| Entropy =
| HeatCapacity = }}

| Section5 = {{Chembox Hazards
| MainHazards = Harmful, Explosive
| FlashPt =
| Autoignition = }}
| Section8 = {{Chembox Related
| OtherAnions =
| OtherCations =
| OtherFunctn =
| Function =
| OtherCpds = [[Hydrazoic acid]], [[Chlorine azide]], [[Methyl azide]] }}
}}

'''Ethyl azide''' C2H5N3 is an explosive compound sensitive to rapid heating, shock or impact. It has exploded when heated to room temperature.<ref>{{cite journal | last1 =Campbell | first1 =Hallock C. | last2 =Rice | first2 =O. K. | journal =Journal of the American Chemical Society | volume =57 | pages =1044 | year =1935 | doi =10.1021/ja01309a019}}</ref><ref>{{cite journal | last1 =Rice | first1 =O. K. | last2 =Campbell | first2 =Hallock C. | title =The Explosion of Ethyl Azide in the Presence of Diethyl Ether | journal =The Journal of Chemical Physics | volume =7 | pages =700 | year =1939 | doi =10.1063/1.1750516}}</ref> When heated to decomposition it emits toxic fumes of [[NOx]].<ref>{{cite journal | last1 =Rice | first1 =O. K. | title =The Role of Heat Conduction in Thermal Gaseous Explosions | journal =The Journal of Chemical Physics | volume =8 | pages =727 | year =1940 | doi =10.1063/1.1750808}}</ref><ref>{{cite journal | last1 =Costa Cabral | first1 =B. J. | last2 =Costa | first2 =M. L. | last3 =Almoster Ferreira | first3 =M. A. | title =ChemInform Abstract: Molecular Structure and Ionization Energies of Azides: an ab initio Study of Hydrazoic Acid, Methyl Azide and Ethyl Azide | journal =ChemInform | volume =24 | pages =no | year =2010 | doi =10.1002/chin.199337053}}</ref>

It is irritating to eyes, respiratory system and skin.

==Uses==
Ethyl azide is used in [[organic synthesis]].

==References==
{{reflist}}

[[Category:Azides]]
[[Category:Explosive chemicals]]

[[de:Ethylazid]]

Ethylazid

2011-02-01T08:49:14Z

{{chembox
| verifiedrevid = 411090573
| ImageFile =
| ImageSize =
| IUPACName =Azidoethane
| OtherNames = Ethane, azido-; 1-Azidoethane
| Section1 = {{Chembox Identifiers
| CAS No 871-31-8
| UN Number =
| PubChem =
| SMILES =
}}
| Section2 = {{Chembox Properties
| Formula = C2H5N3
| MolarMass = 71.08
| Appearance = liquid
| Density =
| MeltingPt =
| BoilingPt = 50
| Solubility =
| SolubleOther =
}}
| Section3 = {{Chembox Explosive
| ShockSens = High
| FrictionSens = High
| ExplosiveV =
| REFactor = }}
| Section4 = {{Chembox Thermochemistry
| DeltaHc =
| DeltaHf = 266.872
| Entropy =
| HeatCapacity = }}

| Section5 = {{Chembox Hazards
| MainHazards = Harmful, Explosive
| FlashPt =
| Autoignition = }}
| Section8 = {{Chembox Related
| OtherAnions =
| OtherCations =
| OtherFunctn =
| Function =
| OtherCpds = [[Hydrazoic acid]], [[Chlorine azide]], [[Methyl azide]] }}
}}

'''Ethyl azide''' C2H5N3 is an explosive compound sensitive to rapid heating, shock or impact. It has exploded when heated to room temperature.<ref>{{cite journal | last1 =Campbell | first1 =Hallock C. | last2 =Rice | first2 =O. K. | journal =Journal of the American Chemical Society | volume =57 | pages =1044 | year =1935 | doi =10.1021/ja01309a019}}</ref><ref>{{cite journal | last1 =Rice | first1 =O. K. | last2 =Campbell | first2 =Hallock C. | title =The Explosion of Ethyl Azide in the Presence of Diethyl Ether | journal =The Journal of Chemical Physics | volume =7 | pages =700 | year =1939 | doi =10.1063/1.1750516}}</ref> When heated to decomposition it emits toxic fumes of [[NOx]].<ref>{{cite journal | last1 =Rice | first1 =O. K. | title =The Role of Heat Conduction in Thermal Gaseous Explosions | journal =The Journal of Chemical Physics | volume =8 | pages =727 | year =1940 | doi =10.1063/1.1750808}}</ref><ref>{{cite journal | last1 =Costa Cabral | first1 =B. J. | last2 =Costa | first2 =M. L. | last3 =Almoster Ferreira | first3 =M. A. | title =ChemInform Abstract: Molecular Structure and Ionization Energies of Azides: an ab initio Study of Hydrazoic Acid, Methyl Azide and Ethyl Azide | journal =ChemInform | volume =24 | pages =no | year =2010 | doi =10.1002/chin.199337053}}</ref>

It is irritating to eyes, respiratory system and skin.

==Uses==
Ethyl azide is used in [[organic synthesis]].

==References==
{{reflist}}

[[Category:Azides]]
[[Category:Explosive chemicals]]

[[de:Ethylazid]]

Natriumthiopental

2011-01-24T16:17:32Z

CheMoBot: Updating {{drugbox}} (changes to verified fields - updated 'StdInChI_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report errors or [[us

{{drugbox | Verifiedfields = changed
| verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| alt = 1:1 mixture (racemate)
| width = 113
| image2 = Sodium-thiopental-3D-vdW-2.png
| StdUNII_Ref = {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| StdInChI_Ref = {{stdinchicite|changed|chemspider}}
| StdInChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| InChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
| CAS_number = 71-73-8
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = DB00599
| C = 11 | H = 17 | N = 2 | Na = 1 | O = 2 | S = 1
| molecular_weight = 264.32 g/mol
| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg [[pancuronium dibromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for [[pancuronium]] dibromide (Pavulon) are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given, placing the subject into a rapidly induced coma. Executions using the three drug combination are usually effective in approximately 10 minutes, but have been known to take several times this amount of time. The use of thiopental alone is hypothesized to cause death in approximately 45 minutes.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental has been the cause of current Supreme Court challenges to the lethal injection protocol, after a study in the medical journal ''[[The Lancet]]'', where autopsy studies on executed inmates revealed that there was not a high enough concentration of thiopental in their blood to have caused unconsciousness.

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. The execution took 43 minutes and was concluded at 11:47 a.m., including approximately 30 minutes to complete the process of inserting the needle, and about 10 minutes between administering the single dose and the pronouncement of death.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref> Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead 8 minutes after the time of injection.<ref>{{cite news | url = http://www.timesfreepress.com/news/2010/jan/07/ohio-executes-man-second-use-1-drug-method/ | title = Ohio executes man in second use of 1-drug method | publisher = [[Chattanooga Times Free Press]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref> A third man was executed using the single-drug method on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref> Most recently, [[William Garner]] was executed in Ohio with sodium thiopental. <ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure." <ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref> On January 21, 2011, the company announced that it would stop production of sodium thiopental from its plant in Italy because it could not guarantee Italian authorities that the drug would not be used in executions. Italy was the only viable place where the company could produce sodium thiopental, leaving the United States without a supplier. <ref> {{cite news | url=http://www.foxnews.com/us/2011/01/21/drug-maker-discontinues-key-death-penalty-drug/#ixzz1BhqUFIxP | title=U.S. Drug Maker Discontinues Key Death Penalty Drug | publisher=Fox News | date=21 January 2011}}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a [[truth drug|truth serum]] to weaken the resolve of the subject and make him more compliant to pressure.<ref name="SMH_truth_serum">{{cite news|url=http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html|publisher=Sydney Morning Herald|title=Truth serum used on 'serial child killers'|date=January 12, 2007|agency=Reuters}}</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the truth. However, the reliability of confessions made under thiopental is dubious; the drug tends to make subjects chatty and cooperative with interrogators.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 137 | pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of STP is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>{{cite web|url=http://www.emedicinehealth.com/drug-thiopental/article_em.htm|title=Pentothal (thiopental)|date=April 12, 2009|publisher=eMedicineHealth}}</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>{{cite journal|last=Steinhaus|first=John E|url=http://www.asahq.org/~/media/For%20Members/Publications/Periodicals/ASA%20Newsletter/NL%20Archives/2001/09%20Sept%2001.ashx|title=The Investigator and His 'Uncompromising Scientific Honesty'|publisher=American Society of Anesthesiologists|journal=ASA NEWSLETTER|month=September|year=2001|volume=65|issue=9|pages=7–9}}</ref> Three months later,<ref>{{cite journal|url=http://www.aana.com/Resources.aspx?id=1811|title=From this point in time: Some memories of my part in the history of anesthesia|first=John S.|last=Lundy|year=1966|journal=Journal of the American Association of Nurse Anesthetists|publisher=American Association of Nurse Anesthetists|volume=24|issue=2|pages=95–102}}</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>{{cite book|url=http://www.aana.com/Resources.aspx?id=1730|title=History of Anesthesia with Emphasis on the Nurse Specialist|last=Thatcher|first=Virginia S.|year=1953|publisher=J.B. Lippincott|chapter=Chapter 7: Illegal or Legal?|chapterurl=http://www.aana.com/uploadedFiles/Resources/Archives_-_Library/Historical_Resources/Thatcher/0008CHP7.PDF}}</ref> Abbott continued to make the drug until 2004, when it spun off its hospital-products division as Hospira.

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless only 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]


[[ar:بنتوثال الصوديوم]]
[[ca:Thiopental]]
[[cs:Thiopental sodný]]
[[de:Thiopental]]
[[es:Tiopentato de sodio]]
[[eo:Tiopentalo]]
[[fr:Thiopental]]
[[it:Tiopental sodico]]
[[hu:Tiopentál-nátrium]]
[[nl:Natriumthiopental]]
[[ja:チオペンタール]]
[[no:Tiopental]]
[[pl:Tiopental]]
[[pt:Tiopental]]
[[ru:Тиопентал натрия]]
[[fi:Tiopentaali]]
[[sv:Tiopental]]
[[tr:Pentotal]]
[[ur:تھایوپینٹال سوڈیئم]]
[[zh:硫噴妥鈉]]

1,2-Bis(dimethylphosphino)ethan

2011-01-21T02:22:37Z

CheMoBot: Updating {{chembox}} (changes to watched fields - updated 'UNII_Ref', 'StdInChI_Ref', 'StdInChIKey_Ref', 'ChEMBL_Ref', 'KEGG_Ref') per Chem/Drugbox validation (report [[Wikipedia_talk:WikiProject

{{chembox
| Watchedfields = changed
| verifiedrevid = 399180057
| Name = 1,2-Bis(dimethylphosphino)ethane
| OtherNames = DMPE ethylenebis(dimethylphosphine) 1,2-Bis(dimethylphosphino)ethane
| ImageFile = dmpe-2D-skeletal-B.png

| ImageName =
| ImageFile1 = Dmpe-from-xtal-1997-3D-balls.png

| ImageName1 =
| IUPACName = Ethane-1,2-diylbis(dimethylphosphane)
| Section1 = {{Chembox Identifiers
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 124423
| InChI = 1/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| SMILES = P(C)(C)CCP(C)C
| InChIKey = ZKWQSBFSGZJNFP-UHFFFAOYAN
| PubChem = 141059
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI = 1S/C6H16P2/c1-7(2)5-6-8(3)4/h5-6H2,1-4H3
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = ZKWQSBFSGZJNFP-UHFFFAOYSA-N
| CASNo = 23936-60-9
}}
| Section2 = {{Chembox Properties
| Formula = C6H16P2
| MolarMass = 150.14 g mol−1
| BoilingPt = 180 °C
| Density = 0.9 g/mL at 25 °C
}}
}}

'''1,2-Bis(dimethylphosphino)ethane''' ('''dmpe''') is a [[diphosphine ligand]] in [[coordination chemistry]]. It can be synthesised by the reaction of [[Grignard reagent|methylmagnesium iodide]] with 1,2-bis(dichlorophosphino)ethane:<ref>{{ cite journal | author = R. J. Burt, J. Chatt, W. Hussain, G. J. Leigh | title = A convenient synthesis of 1,2-bis(dichlorophosphino)ethane, 1,2-bis(dimethylphosphino)ethane and 1,2-bis(diethylphosphino)ethane | journal = [[Journal of Organometallic Chemistry|J. Organomet. Chem.]] | volume = 182 | issue = 2 | year = 1979 | pages = 203–206 | doi = 10.1016/S0022-328X(00)94383-3 }}</ref>

:Cl2PCH2CH2PCl2 + 4MeMgI → Me2PCH2CH2PMe2 + 4MgICl

==References==
<references/>

{{DEFAULTSORT:Bis(dimethylphosphino)ethane}}
[[Category:Chelating agents]]
[[Category:Tertiary phosphines]]

Natriumthiopental

2010-12-30T15:43:03Z

CheMoBot: Updating {{drugbox}} (no changed fields - updated 'StdInChI_Ref') per Chem/Drugbox validation (report errors or bugs)

{{drugbox | verifiedrevid = 402785204
| IUPAC_name = (''RS'')-[5-ethyl-4,6-dioxo-5-(pentan-2-yl)-1,4,5,6-tetrahydropyrimidin-2-yl]sulfanide sodium
| image = tiopental.png
| alt = 1:1 mixture (racemate)
| width = 113
| image2 = Sodium-thiopental-3D-vdW-2.png
| StdUNII_Ref = {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|correct|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|changed|FDA}}= {{fdacite|correct|FDA}}
| UNII = 49Y44QZL70
| InChI = 1S/C11H18N2O2S.Na/c1-4-6-7(3)11(5-2)8(14)12-10(16)13-9(11)15;/h7H,4-6H2,1-3H3,(H2,12,13,14,15,16);/q;+1/p-1
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| StdInChIKey = AWLILQARPMWUHA-UHFFFAOYSA-M
| smiles = [Na+].O=C1NC(=S)/N=C(/[O-])C1(C(C)CCC)CC
| CAS_number = 71-73-8
| CASNo_Ref = {{cascite|correct|CAS}}
| CAS_supplemental = (sodium salt) 76-75-5 (free acid) 
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| ChemSpiderID = 2272257
| ATC_prefix = N01
| ATC_suffix = AF03
| ATC_supplemental = {{ATC|N05|CA19}}
| PubChem = 3000714
| DrugBank = DB00599
| C = 11 | H = 17 | N = 2 | Na = 1 | O = 2 | S = 1
| molecular_weight = 264.32 g/mol
| bioavailability =
| metabolism =
| elimination_half-life = 5.5<ref>{{cite journal |author=Russo H, Brès J, Duboin MP, Roquefeuil B |title=Pharmacokinetics of thiopental after single and multiple intravenous doses in critical care patients |journal=Eur. J. Clin. Pharmacol. |volume=49 |issue=1-2 |pages=127–37 |year=1995 |pmid=8751034 |doi= 10.1007/BF00192371|url= |accessdate=2008-07-18}}</ref>-26 hours<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |month=June |pmid=7235275 |doi= 10.1097/00000542-198106000-00006|url= |accessdate=2008-07-18}}</ref>
| excretion =
| pregnancy_category =
| legal_US = Schedule III
| routes_of_administration = Oral, intravenous
}}
'''Sodium thiopental''', better known as '''Sodium Pentothal''' (a [[trademark]] of [[Abbott Laboratories]]), '''thiopental''', '''thiopentone''' '''sodium''', or '''Trapanal''' (also a trademark), is a rapid-onset short-acting [[barbiturate]] [[general anaesthetic]]. Thiopental is a core medicine in the [[World Health Organization]]'s "[[WHO Model List of Essential Medicines|Essential Drugs List]]", which is a list of minimum medical needs for a basic healthcare system.<ref name="essentialWHO">{{cite web
| year = March 2005
| url = http://whqlibdoc.who.int/hq/2005/a87017_eng.pdf
| title = WHO Model List of Essential Medicines
| format = PDF
| publisher = World Health Organization
| accessdate = 2006-03-12
}}</ref>


==Barbiturates==
{{Main|Barbiturate}}
Barbiturates are a class of drugs that act on the [[GABA A receptor|GABAA receptor]] in the brain and spinal cord. The GABAA receptor is an inhibitory channel that decreases neuronal activity, and barbiturates enhance the inhibitory action of the GABAA receptor. Barbiturates, [[benzodiazepine]]s, and [[alcohol]] all bind to the GABAA receptor. Barbiturates that act on the barbiturate binding site of the GABAA receptor directly gate the chloride ion channel of the GABAA receptor, whereas benzodiazepines acting on the benzodiazepine site on the GABAA receptor increase the opening frequency of the chloride ion channel. This explains why overdoses of barbiturates may be lethal whereas overdoses of benzodiazepines alone are typically not lethal. Another explanation is that barbiturates can activate GABA receptors in the absence of the GABA molecule, whereas benzodiazepines need GABA to be present to have an effect: this may explain the more widespread effects of barbiturates in the central nervous system. Barbiturates have [[anesthetic]], [[sedative]], [[anxiolytic]], [[anticonvulsant]] and [[hypnotic]] properties. Barbiturates do not have [[analgesic]] effects.<ref>{{cite web |url=http://www.healthsystem.virginia.edu/internet/ccm/Anesth/aneshome.cfm |title=Anesthesia and Analgesia |accessdate=2007-08-05 |publisher=[[University of Virginia School of Medicine]]}}</ref>

Further, barbiturates are relatively "promiscuous" (i.e. non-selective) compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nACHR channel, the 5HT3R channel, the GlyR channel and others. Surprisingly, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nACHR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.<ref name="Weber_nAChR_anaesthetics">{{cite journal | last1 = Weber | first1 = M | last2 = Motin | first2 = L | last3 = Gaul | first3 = S | last4 = Beker | first4 = F | last5 = Fink | first5 = RH | last6 = Adams | first6 = DJ | year = 2005 | month = January | title = Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons. | journal = [[British Journal of Pharmacology]] | volume = 144 | issue = 1 | pages = 98–107 | pmid = 15644873 | doi = 10.1038/sj.bjp.0705942 | pmc = 1575970}}</ref> Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.<ref name="Franks_Lieb_general_anaesthetics">{{cite journal | last1 = Franks | first1 = NP | last2 = Lieb | first2 = WR | date = 23 November 1998 | title = Which molecular targets are most relevant to general anaesthesia? | journal = Toxicology Letters | volume = 100–101 | pages = 1–8 | pmid = 10049127 | doi = 10.1016/S0378-4274(98)00158-1}}</ref>

==Uses==
===Anesthesia===
Thiopental is an ultra-short-acting barbiturate and has been used commonly in the induction phase of [[general anaesthesia|general anesthesia]]. Its use in the United States and elsewhere has been largely replaced with that of [[propofol]]. Following [[intravenous therapy|intravenous]] [[Injection (medicine)|injection]] the drug rapidly reaches the brain and causes unconsciousness within 30–45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body and in about 5–10 minutes the concentration is low enough in the brain such that consciousness returns.{{citation needed|date=December 2009}}

A normal dose of thiopental (usually 4–6 mg/kg) given to a pregnant woman for operative delivery ([[caesarian section]]) rapidly makes her unconscious, but the baby in her [[uterus]] remains conscious. However, larger or repeated doses can depress the baby.{{citation needed|date=December 2009}}

Thiopental is not used to maintain anesthesia in surgical procedures because, in infusion, it displays [[Zero order kinetics|zero-order elimination kinetics]], leading to a long period before consciousness is regained. Instead, anesthesia is usually maintained with an [[Inhalational anaesthetic|inhaled anesthetic]] (gas) agent. Inhaled anesthetics are eliminated relatively quickly, so that stopping the inhaled anesthetic will allow rapid return of consciousness. Thiopental would have to be given in large amounts to maintain an anesthetic plane, and because of its 11.5–26 hour [[Biological half-life|half-life]], consciousness would take a long time to return.<ref>{{cite journal |author=Morgan DJ, Blackman GL, Paull JD, Wolf LJ |title=Pharmacokinetics and plasma binding of thiopental. II: Studies at cesarean section |journal=Anesthesiology |volume=54 |issue=6 |pages=474–80 |year=1981 |pmid=7235275 |doi=10.1097/00000542-198106000-00006}}</ref>

In [[veterinary medicine]], thiopental is used to induce [[Veterinary anesthesia|anesthesia in animals]]. Since thiopental is redistributed to fat, certain breeds of dogs – primarily the [[sight hounds]] – can have prolonged recoveries from thiopental due to their lack of body fat and their lean body mass. Thiopental is always administered intravenously, as it can be fairly irritating; severe [[tissue necrosis]] and sloughing can occur if it is injected incorrectly into the tissue around a vein.

===Medically induced coma===
In addition to anesthesia induction, thiopental was historically used to induce medical [[coma]]s. It has now been superseded by drugs such as [[propofol]].

Thiopental has a long Context Sensitive Half Time (CSHT), meaning infusions saturate peripheral compartments (fat, muscle etc.). When the infusion is stopped, the drug redistributes from the peripheral tissues back into the blood, prolonging the effect.

Thiopental also exhibits [[Rate_law#Zero-order_reactions|zero order kinetics]] at higher doses. The rate of elimination becomes constant.

Patients with brain swelling, causing elevation of the intracranial pressure, either secondary to trauma or following surgery, may benefit from this drug. Thiopental, and the barbiturate class of drugs, decrease neuronal activity and therefore decrease the production of osmotically active metabolites, which in turn decreases swelling. Patients with significant swelling have improved outcomes following the induction of coma. Reportedly, thiopental has been shown to be superior to [[pentobarbital]]<ref>{{cite journal |author=Pérez-Bárcena J, Barceló B, Homar J, ''et al.'' |title=[Comparison of the effectiveness of pentobarbital and thiopental in patients with refractory intracranial hypertension. Preliminary report of 20 patients] |language=Spanish; Castilian |journal=Neurocirugia (Astur) |volume=16 |issue=1 |pages=5–12; discussion 12–3 |year=2005 |month=February |pmid=15756405 |doi= |url=http://www.revistaneurocirugia.com/web/artics/v16n1/1.pdf |accessdate=2008-07-18}}</ref> in reducing intracranial pressure.

===Euthanasia===
Thiopental is used intravenously for the purposes of [[euthanasia]]. The [[Belgium|Belgian]]s and the [[Netherlands|Dutch]] have created a protocol that recommends sodium thiopental as the ideal agent to induce coma, followed by [[pancuronium bromide]].<ref name=euthanasics>{{cite web |url=http://wweek.com/html/euthanasics.html |title=Administration and Compounding of Euthanasic Agents |accessdate=2008-07-18 |author=Royal Dutch Society for the Advancement of Pharmacy |publisher=[[The Hague]] |year=1994}}</ref>

Intravenous administration is the most reliable and rapid way to accomplish euthanasia and therefore can be safely recommended. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg [[pancuronium dibromide]] (Pavulon) or 20 mg [[vecuronium bromide]] (Norcuron). The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for [[pancuronium]] dibromide (Pavulon) are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg.<ref name=euthanasics />

===Lethal injection===
{{details|Lethal injection}}

Along with [[pancuronium bromide]] and [[potassium chloride]], thiopental is used in 34 states of the [[United States|U.S.]] to execute prisoners by [[lethal injection]]. A very large dose is given, placing the subject into a rapidly induced coma. Executions using the three drug combination are usually effective in approximately 10 minutes, but have been known to take several times this amount of time. The use of thiopental alone is hypothesized to cause death in approximately 45 minutes.<ref name="Biros">{{cite web
| year = December 2001
| url = http://www.breitbart.com/article.php?id=D9CF8Q2G6&show_article=1&catnum=0
| title = Ohio executes inmate with 1-drug lethal injection
| publisher = AP
| accessdate = 2009-12-08
}} </ref> The use of sodium thiopental has been the cause of current Supreme Court challenges to the lethal injection protocol, after a study in the medical journal ''[[The Lancet]]'', where autopsy studies on executed inmates revealed that there was not a high enough concentration of thiopental in their blood to have caused unconsciousness.

Following a shortage that led a court to delay an execution in California, a company spokesman for [[Hospira]], the sole American manufacturer of the drug, expressed strong reservations about the use of thiopental in the lethal injection procedure. "Hospira manufactures this product because it improves or saves lives, and the company markets it solely for use as indicated on the product labeling. The drug is not indicated for capital punishment, and Hospira does not support its use in this procedure." <ref>{{cite news | url = http://www.nytimes.com/2010/09/29/us/29execute.html | title = Judges Question California's Motivation on Execution | first = Jesse | last = McKinley | date = 28 September 2010 | work = [[New York Times]]}}</ref>

On December 8, 2009, the State of Ohio became the first to use a single dose of sodium thiopental for its capital execution, following the failed use of the standard three-drug cocktail during a recent execution, due to inability to locate suitable veins. [[Kenneth Biros]] was executed using the single-drug method. The execution took 43 minutes and was concluded at 11:47 a.m., including approximately 30 minutes to complete the process of inserting the needle, and about 10 minutes between administering the single dose and the pronouncement of death.<ref>{{cite news | url = http://www.cbsnews.com/blogs/2009/09/24/crimesider/entry5334823.shtml | title = Kenneth Biros Execution: Ohio Man First to Die Under 1-Drug Thiopental Sodium Method | first = Edecio | last = Martinez | date = 8 December 2009 | work = [[CBS News]]}}</ref><ref>{{cite news | url = http://www.google.com/hostednews/ap/article/ALeqM5h18cDX6PuFXpdEc3JIHpQRFMapvAD9CF8BL00 | title = Ohio executes inmate with 1-drug lethal injection | date = 9 December 2009 | agency = [[Associated Press]] | publisher = [[Google]] | archiveurl = http://www.webcitation.org/5mEkZTdUI | archivedate = 23 December 2009}}</ref>

The state of Ohio executed a second man using sodium thiopental on January 7, 2010. [[Vernon Smith (murderer)|Vernon Smith]] was pronounced dead 8 minutes after the time of injection.<ref>{{cite news | url = http://www.chron.com/disp/story.mpl/ap/top/all/6803389.html | title = Ohio executes man in second use of 1-drug method | work = [[Houston Chronicle]] | first = Julie Carr | last = Smyth | agency = [[Associated Press]] | date = 7 January 2010}}</ref>

The state of Ohio executed a third man using sodium thiopental on April 20, 2010. [[Daryl Durr]] was pronounced dead at 10:36 am.<ref>{{cite news | url = http://www.cnn.com/2010/CRIME/04/20/ohio.execution/index.html?hpt=Sbin | title = Ohio executes murderer of teen | work = [[CNN.com]] | date = 20 April 2010 }}</ref>

Most recently, [[William Garner]] was executed in Ohio with sodium thiopental. <ref> {{cite news | url = http://www.cnn.com/2010/CRIME/07/13/ohio.execution/index.html?iref=NS1 | title = Man convicted of murdering 5 children executed in Ohio | work = [[CNN.com]] | date = 13 July 2010 }}</ref>

The [[Washington (U.S. state)|state of Washington]] is now the second state in the U.S. to use the single-dose sodium thiopental injections for death penalty executions. On September 10, 2010, [[Cal Coburn Brown]] was executed. His was the first execution in the state to use a single dose, single drug injection. His death was pronounced approximately one and a half minutes after the intravenous administration of five grams of the drug.<ref> {{cite news | url = http://seattletimes.nwsource.com/html/localnews/2012856652_execution10m.html | title = Killer on death row 16-1/2 years is executed | work = [[The Seattle Times]] | date = 10 September 2010 | first=Jennifer | last=Sullivan}}</ref>

===Truth serum===
Thiopental (Pentothal) is still used in some places as a "[[truth drug|truth serum]]", to weaken the resolve of the subject and make him more compliant to pressure.<ref name="SMH_truth_serum">[http://www.smh.com.au/news/world/truth-serum-used-on-serial-child-killers/2007/01/12/1168105166282.html Sydney Morning Herald], Truth serum used on 'serial child killers', January 12, 2007, Reuters.</ref> The barbiturates as a class decrease higher cortical brain functioning. Some psychiatrists hypothesize that because lying is more complex than telling the truth, suppression of the higher cortical functions may lead to the uncovering of the "truth". However, the reliability of confessions made under thiopental is dubious; the drug tends to make subjects chatty and cooperative with interrogators.<ref>{{cite book |author=Anne Bannon; Stevens, Serita Deborah |title=The Howdunit Book of Poisons (Howdunit) |publisher=Writers Digest Books |location=Cincinnati |year=2007 |isbn=1-58297-456-X}}</ref>

===Psychiatry===
Psychiatrists have used thiopental to desensitize patients with [[phobia]]s,<ref>{{cite journal | url = http://ajp.psychiatryonline.org/cgi/content/abstract/137/12/1580 | title = Behavioral desensitization of phobic anxiety using thiopental sodium | first = T. | last = Pearlman | journal = [[The American Journal of Psychiatry]] | publisher = [[American Psychiatric Association]] | year = 1980 | issue = 137 | pages = 1580–1582 | pmid = 6108082 | volume = 137}}</ref> and to "facilitate the recall of painful repressed memories."<ref>{{cite news | url = http://www.time.com/time/magazine/article/0,9171,863001,00.html | title = Drugged Future? | date = February 24, 1958 | work = [[TIME]]}}</ref> One psychiatrist who worked with thiopental is the [[Dutch people|Dutch]] Professor Jan Bastiaans, who used this procedure to help release trauma in victims of the [[Nazi]]s.<ref>{{cite journal | url = http://www.maps.org/news-letters/v08n1/08118sne.html | title = The LSD Therapy Career of Jan Bastiaans, M.D. | first = Stephen | last = Snelders | journal = Newsletter of the Multidisciplinary Association for Psychedelic Studies | publisher = [[Multidisciplinary Association for Psychedelic Studies]] | volume = 8 | issue = 1 | year = 1998 | pages = 18–20}}</ref>

==Metabolism==
As with all lipid-soluble anaesthetic drugs, the short duration of action of STP is due almost entirely to its redistribution away from central circulation towards muscle and fat tissue. Once redistributed, the free fraction in the blood is metabolised in the liver. Sodium thiopental is mainly metabolized to [[pentobarbital]],<ref>{{cite journal |author=WINTERS WD, SPECTOR E, WALLACH DP, SHIDEMAN FE |title=Metabolism of thiopental-S35 and thiopental-2-C14 by a rat liver mince and identification of pentobarbital as a major metabolite |journal=J. Pharmacol. Exp. Ther. |volume=114 |issue=3 |pages=343–57 |year=1955 |month=July |pmid=13243246 |doi= |url=http://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=13243246 |accessdate=2008-07-18}} {{Dead link|date=September 2010|bot=H3llBot}}</ref> 5-ethyl-5-(1'-methyl-3'-hydroxybutyl)-2-thiobarbituric acid, and 5-ethyl-5-(1'-methyl-3'-carboxypropyl)-2-thiobarbituric acid.<ref>{{cite journal |author=Bory C, Chantin C, Boulieu R, ''et al.'' |title=[Use of thiopental in man. Determination of this drug and its metabolites in plasma and urine by liquid phase chromatography and mass spectrometry] |language=French |journal=C. R. Acad. Sci. III, Sci. Vie |volume=303 |issue=1 |pages=7–12 |year=1986 |pmid=3093002 |doi= |url= |accessdate=2008-07-18}}</ref>

==Dosage==
The usual dose range for induction of anesthesia using thiopental is from 3 to 7 mg/kg; however, there are many factors that can alter this. Premedication with sedatives such as [[benzodiazepines]] or [[clonidine]] will reduce requirements, as do specific disease states and other patient factors. Among patient factors are: age, sex, lean body mass. Specific disease conditions that can alter the dose requirements of thiopentone and for that matter any other intravenous anaesthetic are: [[hypovolemia]], burns, [[azotemia]], [[hepatic failure]], [[hypoproteinemia]], etc.

==Side effects==
As with nearly all [[anesthesia|anesthetic]] [[Medication|drug]]s, thiopental causes cardiovascular and respiratory depression resulting in [[hypotension]], [[apnea]] and [[airway]] obstruction. For these reasons, only suitably trained medical personnel should give thiopental in an environment suitably equipped to deal with these effects. Side effects include headache, [[delirium|emergence delirium]], prolonged [[somnolence]], and [[nausea]]. Intravenous administration of sodium thiopental is followed instantly by an odor and/or taste sensation, sometimes described as being similar to rotting onions, or to garlic. The hangover from the side effects may last up to 36 hours.

Although individual [[molecules]] of thiopental contain one [[sulfur]] atom, it is not a [[sulfonamide (chemistry)|sulfonamide]], and does not show allergic reactions of sulfa/sulpha drugs.

==Contraindications==
Thiopental should not be given in case of [[liver disease]], [[Addison's disease]], [[myxedema]], severe [[heart disease]], severe [[hypotension]], a severe [[breathing disorder]], or a history of [[porphyria]].<ref>[http://www.emedicinehealth.com/drug-thiopental/article_em.htm eMedicineHealth > thiopental (pentothal)]. Revision date: 4/12/2009.</ref>

Co-administration of [[pentoxifylline]] and thiopental causes death by acute [[pulmonary oedema]] in rats. This pulmonary oedema was not mediated by [[cardiac failure]] or by [[pulmonary hypertension]] but was due to increased pulmonary vascular permeability.<ref>{{cite journal |author=Pereda J, Gómez-Cambronero L, Alberola A, ''et al.'' |title=Co-administration of pentoxifylline and thiopental causes death by acute pulmonary oedema in rats |journal=Br. J. Pharmacol. |volume=149 |issue=4 |pages=450–5 |year=2006 |month=October |pmid=16953192 |pmc=1978439 |doi=10.1038/sj.bjp.0706871 |accessdate=2008-07-18}}</ref>

==History==
Sodium thiopental was discovered in the early 1930s by [[Ernest H. Volwiler]] and Donalee L. Tabern, working for [[Abbott Laboratories]]. It was first used in human beings on March 8, 1934, by Dr. Ralph M. Waters<ref>{{cite web | url = http://www.anesthesia.wisc.edu/AHA/Calendar/March.html | title = This Month in Anesthesia History: March | publisher = Anesthesia History Association}}</ref> in an investigation of its properties, which were short-term anesthesia and surprisingly little analgesia.<ref>Steinhaus, John E. [http://www.asahq.org/Newsletters/2001/09_01/steinhaus.htm The Investigator and His ‘Uncompromising Scientific Honesty’] American Society of Anesthesiologists. ''NEWSLETTER.'' September 2001, Volume 65, Number 9.</ref> Three months later,<ref>[http://www.aana.com/archives/imagine/1997/08imagine97.asp Imagining in Time—''From this point in time: Some memories of my part in the history of anesthesia—John S. Lundy, MD''] August 1997, AANA Archives-Library</ref> Dr. John S. Lundy started a clinical trial of thiopental at the [[Mayo Clinic]] at the request of Abbott.<ref>[http://www.aana.com/archives/pdf/0008CHP7.pdf History of Anesthesia with Emphasis on the Nurse Specialist] ''Archives of the American Association of Nurse Anesthetists.'' 1953</ref>

Thiopental is famously associated with a number of anesthetic deaths in victims of the attack on [[Pearl Harbor]]. These deaths, relatively soon after the substance's discovery, were due to excessive doses given to shocked trauma patients. Evidence has become available through freedom of information legislation and has been reviewed in the "British Journal of Anaesthesia".<ref name="pmid7547061">{{cite journal |author=Bennetts FE |title=Thiopentone anaesthesia at Pearl Harbor |journal=Br J Anaesth |volume=75 |issue=3 |pages=366–8 |year=1995 |month=September |pmid=7547061 |doi= |url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=7547061 |accessdate=2008-07-18}}</ref> Thiopental anaesthesia was in its early days, but nevertheless only 13 of 344 wounded admitted to the [[Tripler Army Medical Center|Tripler Army Hospital]] did not survive.

Thiopental is still rarely used as a [[recreational drug]], usually stolen from veterinarians or other legitimate users of the drug; however, more common sedatives such as [[benzodiazepines]] are usually preferred as recreational drugs, and abuse of thiopental tends to be uncommon and opportunistic.

==References==
{{Reflist|2}}

==External links==
* [http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?sid=149220 PubChem Substance Summary: Thiopental]

{{Barbiturates}}
{{General anesthetics}}
{{Hypnotics and sedatives}}

{{DEFAULTSORT:Sodium Thiopental}}

[[Category:General anesthetics]]
[[Category:Lethal injection components]]
[[Category:Sodium compounds]]
[[Category:Thiobarbiturates]]
[[Category:World Health Organization essential medicines]]


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