Influence of Alcohol on Anesthetic Requirements and Acute Toxicity

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Abstract
The influence of alcohol on the concentrations of halothane necessary to produce anesthesia, respiratory arrest and cardiac failure was studied in rats. The effect of alcohol was investigated in the following circumstances: during acute intoxication, during chronic intoxication, following withdrawal from chronic intoxication and after reintoxication during withdrawal. Significant differences in halothane concentrations between alcohol-treated and control (no exposure to alcohol) rats included halothane concentration in the brain at the onset of anesthesia during acute intoxication (12.2 mg/100 g) and following withdrawal from chronic intoxication (38.1 mg/100 g) compared with control rats (27.8 mg/100 g); halothane concentration in the brain at the onset of respiratory arrest during acute intoxication (49.5 mg/100 g) and during chronic intoxication (55.6 mg/100 g) compared with control rats (63.6 mg/100 g); and halothane concentration in the heart at the onset of cardiac failure during acute intoxication (45.4 mg/100 g), during chronic intoxication (67.6 mg/100 g) and after reintoxication (61.6 mg/100 g) compared with control rats (81.6 mg/100 g). Acute and chronic intoxication with alcohol should be viewed as separate entities with respect to their influence on halothane anesthesia. Acute administration of alcohol reduces anesthetic requirements more than it reduces the toxic concentrations of halothane. Chronic administration of an adequate quantity of alcohol produces tolerance to its own anesthetic, respiratory and cardiac effects. This tolerance is more marked with regard to respiratory depression than it is to anesthesia and cardiac depression. Alcohol produces cross-tolerance to the anesthetic effects of halothane. Tolerance to the 3 studied effects persists in varying degrees after withdrawal; cross-tolerance persists only to the anesthetic effects of halothane. The marked quantitative differences between the anesthetic, respiratory and cardiac interactions between alcohol and halothane suggest that the extent of one interaction must not be used to predict the extent of another.

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