Ryle P R, Chakraborty J, Thomson A D
Alcohol Alcohol. 1985;20(3):287-91.
Naloxone hydrochloride (2.0 mg/kg) has been found to reverse the significant decreases in the hepatic cytosolic and mitochondrial [NAD+]/[NADH] ratios observed after acute ethanol administration in rats. This correction of the ethanol-induced changes in the hepatocellular redox state by naloxone was, however, not associated with any lowering of serum ethanol concentrations or an observable reduction in the extent of intoxication. This lack of antagonism of alcohol intoxication by naloxone was not affected by the feeding status of the animals, the time point after naloxone administration at which serum ethanol concentration was determined or the method used for ethanol analysis. Thus this study has failed to confirm that naloxone antagonises acute alcohol intoxication, in spite of its potent ability to reverse the ethanol-induced changes in the hepatic redox state.
已发现盐酸纳洛酮(2.0毫克/千克)可逆转大鼠急性乙醇给药后观察到的肝细胞溶质和线粒体中[NAD+]/[NADH]比值的显著下降。然而,纳洛酮对乙醇诱导的肝细胞氧化还原状态变化的这种纠正,与血清乙醇浓度的任何降低或中毒程度的明显减轻均无关。纳洛酮对酒精中毒缺乏拮抗作用,不受动物的喂养状态、测定血清乙醇浓度时纳洛酮给药后的时间点或乙醇分析所用方法的影响。因此,尽管纳洛酮具有逆转乙醇诱导的肝脏氧化还原状态变化的强大能力,但本研究未能证实纳洛酮可拮抗急性酒精中毒。