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Review
. 2003 Sep;97(3):718-740.
doi: 10.1213/01.ANE.0000081063.76651.33.

Inhaled anesthetics and immobility: mechanisms, mysteries, and minimum alveolar anesthetic concentration

James M Sonner  1 , Joseph F Antognini, Robert C Dutton, Pamela Flood, Andrew T Gray, R Adron Harris, Gregg E Homanics, Joan Kendig, Beverley Orser, Douglas E Raines, James Trudell, Bryce Vissel, Edmond I Eger 2nd
Affiliations
Review

Inhaled anesthetics and immobility: mechanisms, mysteries, and minimum alveolar anesthetic concentration

James M Sonner et al. Anesth Analg. 2003 Sep.

Erratum in

  • Anesth Analg. 2004 Jan;98(1):29

Abstract

Studies using molecular modeling, genetic engineering, neurophysiology/pharmacology, and whole animals have advanced our understanding of where and how inhaled anesthetics act to produce immobility (minimum alveolar anesthetic concentration; MAC) by actions on the spinal cord. Numerous ligand- and voltage-gated channels might plausibly mediate MAC, and specific amino acid sites in certain receptors present likely candidates for mediation. However, in vivo studies to date suggest that several channels or receptors may not be mediators (e.g., gamma-aminobutyric acid A, acetylcholine, potassium, 5-hydroxytryptamine-3, opioids, and alpha(2)-adrenergic), whereas other receptors/channels (e.g., glycine, N-methyl-D-aspartate, and sodium) remain credible candidates.

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