Influence of Alcohol on Anesthetic Requirements and Acute Toxicity
Influence of Alcohol on Anesthetic Requirements and Acute Toxicity
复制标题
酒精对麻醉需求和急性毒性的影响
作者：
B. Wolfson;B. Freed
在大鼠中研究了酒精对产生麻醉、呼吸停止和心力衰竭所需的氟烷浓度的影响。在下列情况下研究酒精的影响：(1)急性中毒期间；(2)慢性中毒期间；(3)慢性中毒戒断后；(4)戒断期间再中毒后。酒精处理大鼠和对照大鼠（未接触酒精）之间氟烷浓度的显著差异包括：(1)与对照大鼠（27.8 mg/100 g）相比，急性中毒期间麻醉开始时脑内氟烷浓度（12.2 mg/100 g）和慢性中毒戒断后（38.1 mg/100 g）；(2)与对照大鼠（63.6 mg/100 g）相比，急性中毒期间呼吸骤停发作时脑内氟烷浓度（49.5 mg/100 g）和慢性中毒期间（55.6 mg/100 g）；(3)与对照大鼠（81.6 mg/100 g）相比，急性中毒时心力衰竭发作时（45.4 mg/100 g）、慢性中毒时（67.6 mg/100 g）和再中毒后（61.6 mg/100 g）心脏氟烷浓度。结果表明，就其对氟烷麻醉的影响而言，急性和慢性酒精中毒应被视为独立的实体。具体来说，酒精的急性施用减少麻醉需求比减少氟烷的毒性浓度更多。长期饮用适量的酒精会产生对酒精本身的麻醉、呼吸和心脏作用的耐受性。这种耐受性在呼吸抑制方面比在麻醉和心脏抑制方面更为明显。酒精也对氟烷的麻醉作用产生交叉耐受性。停药后对三种药物的耐受性仍有不同程度的维持；交叉耐受只对氟烷的麻醉作用有效。酒精和氟烷之间的麻醉、呼吸和心脏相互作用的显著数量差异表明，不能用一种相互作用的程度来预测另一种相互作用的程度。
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: (1) during acute intoxication; (2) during chronic intoxication; (3) following withdrawal from chronic intoxication; and, (4) after reintoxication during withdrawal. Significant differences in halothane concentrations between alcohol-treated and control (no exposure to alcohol) rats included: (1) 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); (2) 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, (3) 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). The results indicate that acute and chronic intoxication with alcohol should be viewed as separate entities with respect to their influence on halothane anesthesia. Specifically, 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 also produces cross-tolerance to the anesthetic effects of halothane. Tolerance to the three 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.