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Inhaled anesthetics and immobility: Mechanisms, mysteries, and minimum alveolar anesthetic concentration ANESTHESIA AND ANALGESIA Sonner, J. M., Antognini, J. F., Dutton, R. C., Flood, P., Gray, A. T., Harris, R. A., Homanics, G. E., Kendig, J., Orser, B., Raines, D. E., Trudell, J., Vissel, B., Eger, E. I. 2003; 97 (3): 718-740

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.

View details for DOI 10.1213/01.ANE.0000081063.76651.33

View details for Web of Science ID 000184890300025

View details for PubMedID 12933393