We investigated the effect of ethanol on adverse effects of anoxia and reoxygenation in isolated rat hearts. Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM), in both anoxic and aerobic perfusion media resulted in a significant reduction of cell injury and inhibition of creatine phosphokinase release. The contraction bands were reduced to 0.24 as compared to 1.14 per field in the non-treated hearts. The tissue CA++ was decreased to 8.72 μmol/gm/dry wt as compared to 20.17 μmol/gm/dry weight in the non-treated hearts and tissue ATP was increased by 50 % in the treated tissue (8.14 μmol/gm/dry wt), as compared to the nontreated anoxic tissue (4.41 μmol/gm/dry wt). However, the inclusion of only ethanol in the anoxic medium did not decrease the damage, suggesting that maximal injury occurred during reoxygenation. Ethanol appears to inhibit myofibril contractures and preserve the structural integrity of plasma membrane during anoxia and reoxygenation. This study suggests a beneficial effect of ethanol in low doses on the post anoxic reperfusion injury in the myocardium.
- cell damage
- creatine phosphokinase
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)