Abstract
The molecular mechanisms which underlie general anesthesia are not clearly understood. First, there are two chemically disparate classes of pharmacologic agents to consider (both intravenous and volatile) which induce general anesthesia. Second, investigators in the field are divided into two differing camps of thought: (1) those who believe that anesthetics work by altering normal membrane fluidity, and (2) those who believe that anesthetics work by perturbing normal protein function. Recently, there is growing evidence that the “perturbed protein” hypothesis holds greater promise over the “altered fluidity” hypothesis in explaining the molecular mechanisms of general anesthesia.1The simplest working idea is that general anesthetics act by binding directly to a particularly sensitive protein, which may or may not be located in a lipid membrane, and inhibiting its normal function.
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