Chemistry:Enflurane

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Short description: Chemical compound
Enflurane
Enflurane.svg
Enflurane-3D-balls.png
Clinical data
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ATC code
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Legal status
  • BR: Class C1 (Other controlled substances)
Pharmacokinetic data
Protein binding97%
Identifiers
CAS Number
PubChem CID
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Chemical and physical data
FormulaC3H2ClF5O
Molar mass184.49 g·mol−1
3D model (JSmol)
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Enflurane (2-chloro-1,1,2-trifluoroethyl difluoromethyl ether) is a halogenated ether. Developed by Ross Terrell in 1963, it was first used clinically in 1966. It was increasingly used for inhalational anesthesia during the 1970s and 1980s[1] but is no longer in common use.[2]

Enflurane is a structural isomer of isoflurane. It vaporizes readily, but is a liquid at room temperature.

Physical properties

Property Value
Boiling point at 1 atm 56.5 °C
MAC 1.68
Vapor pressure at 20 °C 22.9 kPa (172 mm Hg)
Blood:gas partition coefficient 1.9
Oil:gas partition coefficient 98

Pharmacology

The exact mechanism of the action of general anaesthetics has not been delineated.[3] Enflurane acts as a positive allosteric modulator of the GABAA,[4][5][6][7] glycine, and 5-HT3 receptors,[8][9] and as a negative allosteric modulator of the AMPA, kainate, and NMDA receptors,[9][10][11] as well as of nicotinic acetylcholine receptors.[8]

Side effects

Clinically, enflurane produces a dose-related depression of myocardial contractility with an associated decrease in myocardial oxygen consumption. Between 2% and 5% of the inhaled dose is oxidised in the liver, producing fluoride ions and difluoromethoxy-difluoroacetic acid. This is significantly higher than the metabolism of its structural isomer isoflurane.

Enflurane also lowers the threshold for seizures, and should especially not be used on people with epilepsy.[12] Like all potent inhalation anaesthetic agents it is a known trigger of malignant hyperthermia.

Like the other potent inhalation agents it relaxes the uterus in pregnant women which is associated with more blood loss at delivery or other procedures on the gravid uterus.

The obsolete (as an anaesthetic) agent methoxyflurane had a nephrotoxic effect and caused acute kidney injury, usually attributed to the liberation of fluoride ions from its metabolism. Enflurane is similarly metabolised but the liberation of fluoride results in a lower plasma level and enflurane related kidney failure seemed unusual if seen at all.[13]

Occupational safety

The U.S. National Institute for Occupational Safety and Health (NIOSH) has set a recommended exposure limit (REL) for exposure to waste anaesthetic gas of 2 ppm (15.1 mg/m3) over a 60-minute period. Symptoms of occupational exposure to enflurane include eye irritation, central nervous system depression, analgesia, anesthesia, convulsions, and respiratory depression.[14]

References

  1. ↑ Electroencephalography: Basic Principles, Clinical Applications, and Related Fields. Lippincott Williams & Wilkins. 2005. p. 1156. ISBN 978-0-7817-5126-1. https://books.google.com/books?id=tndqYGPHQdEC&pg=PA1156. 
  2. ↑ Pharmacology and Physiology for Anesthesia. 2013. doi:10.1016/C2009-0-41712-4. ISBN 9781437716795. 
  3. ↑ "How does anesthesia work?". Scientific American. 7 February 2005. http://www.scientificamerican.com/article/how-does-anesthesia-work/. 
  4. ↑ "Effects of two volatile anesthetics and a volatile convulsant on the excitatory and inhibitory amino acid responses in dissociated CNS neurons of the rat". Journal of Neurophysiology 66 (6): 2014–2021. December 1991. doi:10.1152/jn.1991.66.6.2014. PMID 1667416. 
  5. ↑ "Enhancement of gamma-aminobutyric acid-activated Cl- currents in cultured rat hippocampal neurones by three volatile anaesthetics". The Journal of Physiology 449: 279–293. April 1992. doi:10.1113/jphysiol.1992.sp019086. PMID 1326046. 
  6. ↑ "The actions of ether, alcohol and alkane general anaesthetics on GABAA and glycine receptors and the effects of TM2 and TM3 mutations". British Journal of Pharmacology 129 (4): 731–743. February 2000. doi:10.1038/sj.bjp.0703087. PMID 10683198. 
  7. ↑ "General anesthetics potentiate gamma-aminobutyric acid actions on gamma-aminobutyric acidA receptors expressed by Xenopus oocytes: lack of involvement of intracellular calcium". The Journal of Pharmacology and Experimental Therapeutics 263 (2): 569–578. November 1992. PMID 1331405. 
  8. ↑ 8.0 8.1 Neurochemistry of Consciousness: Neurotransmitters in Mind. John Benjamins Publishing. 2002. pp. 154–. ISBN 978-1-58811-124-1. https://books.google.com/books?id=3o2fCDDoSuUC&pg=PA154. 
  9. ↑ 9.0 9.1 A Practice of Anesthesia for Infants and Children: Expert Consult - Online and Print. Elsevier Health Sciences. 2013. pp. 499–. ISBN 978-1-4377-2792-0. https://books.google.com/books?id=MAXTnQStL0cC&pg=PA499. 
  10. ↑ Clinical Anesthesia, 7e: Print + Ebook with Multimedia. Lippincott Williams & Wilkins. 7 February 2013. pp. 116–. ISBN 978-1-4698-3027-8. https://books.google.com/books?id=exygUxEuxnIC&pg=PA116. 
  11. ↑ "Enflurane inhibits NMDA, AMPA, and kainate-induced currents in Xenopus oocytes expressing mouse and human brain mRNA". FASEB Journal 7 (5): 479–485. March 1993. doi:10.1096/fasebj.7.5.7681790. PMID 7681790. 
  12. ↑ Enflurane has established ictogenic properties?. April 2004. doi:10.15363/thinklab.d224. https://thinklab.com/discussion/prediction-in-epilepsy/224#6. Retrieved October 17, 2016. 
  13. ↑ Clinical Anesthesiology (3rd ed.). New York: Lange Medical Books/McGraw-Hill. September 2006. p. 142. 
  14. ↑ "CDC - NIOSH Pocket Guide to Chemical Hazards - Enflurane". https://www.cdc.gov/niosh/npg/npgd0253.html. 



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