Inhaled Anesthetics and Immobility: Mechanisms, Mysteries, and Minimum Alveolar Anesthetic Concentration

作者：James M. Sonner, Joseph F. Antognini, Robert C. Dutton, Pamela Dru Flood, Andrew T. Gray, Robert Adron Harris, Gregg E. Homanics, Joan J. Kendig, Beverley Anne Orser, Douglas E. Raines, James R. Trudell, Bryce Vissel, and Edmond I Eger · 发表于：Anesthesia & Analgesia · 年份：2003 · DOI：10.1213/01.ane.0000081063.76651.33 · 被引用次数：327 · 研究领域：Ion channel regulation and function、Neuroscience of respiration and sleep、Anesthesia and Neurotoxicity Research

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.