Moderating effect of low doses of ethanol on reoxygenation injury in the anoxic myocardium.

We have investigated the action of ethanol on the reoxygenation injury in isolated rat hearts. Perfusion of the anoxic Krebs-Henseleit medium for 40 minutes followed by 30 minutes of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mMol), in both anoxic and aerobic perfusion media resulted in a marked reduction of cell injury and inhibition of creatine kinase. Contraction band necrosis was reduced to 0.25 as compared to 1.14 per field in the nontreated hearts. The tissue Ca++ was decreased to 8.2 as compared to 12.12 mumol/g/dry weight in the non-treated hearts and tissue ATP was increased by 50% in the treated tissue (9.33 mumol/g/dry wt) as compared to the non-treated anoxic tissue (5.5 mumol). Thus, ethanol appears to lessen myofibrilar contraction bands and preserve plasma membrane integrity during anoxia and reoxygenation. This suggests a scavenging role of free radicals which include hydroxy radicals or closely related species, in the pathogenesis of anoxic cell injury and beneficial effect of ethanol in low doses on the post anoxic reoxygenation injury.