Is a new paradigm needed to explain how inhaled anesthetics produce immobility? ANESTHESIA AND ANALGESIA Eger, E. I., Raines, D. E., Shafer, S. L., Hemmings, H. C., Sonner, J. M. 2008; 107 (3): 832-848

Abstract

A paradox arises from present information concerning the mechanism(s) by which inhaled anesthetics produce immobility in the face of noxious stimulation. Several findings, such as additivity, suggest a common site at which inhaled anesthetics act to produce immobility. However, two decades of focused investigation have not identified a ligand- or voltage-gated channel that alone is sufficient to mediate immobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5-HT3, gamma-aminobutyric acid type A and glutamate receptors, and potassium and calcium channels appear to be irrelevant or play only minor roles. Furthermore, no combination of actions on ligand- or voltage-gated channels seems sufficient. A few plausible targets (e.g., sodium channels) merit further study, but there remains the possibility that immobilization results from a nonspecific mechanism.

View details for DOI 10.1213/ane.0b013e318182aedb

View details for Web of Science ID 000258702500020

View details for PubMedID 18713892

View details for PubMedCentralID PMC2653203