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Inhaled anesthetics and immobility: mechanisms, mysteries, and minimum alveolar anesthetic concentration Sonner JM; Antognini JF; Dutton RC; Flood P; Gray AT; Harris RA; Homanics GE; Kendig J; Orser B; Raines DE; Trudell J; Vissel B; Eger EI 2ndAnesth Analg 2003[Sep]; 97 (3): 718-740Studies 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.|Anesthetics, Inhalation/administration & dosage/pharmacokinetics/*pharmacology[MESH]|Animals[MESH]|Genetic Engineering[MESH]|Humans[MESH]|In Vitro Techniques[MESH]|Ion Channels/drug effects[MESH]|Models, Molecular[MESH]|Movement/*drug effects[MESH]|Pulmonary Alveoli/*metabolism[MESH]|Spinal Cord/drug effects/physiology[MESH] |
