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Abstract:
It is now well established that consumption of ethyl alcohol, both acute and chronic, exerts deleterious effects on the heart. Evidence is presented that the initial event that precipitates both acute and chronic changes reflects the physical effects of alcohol on membrane phospholipids and perhaps proteins. The presence of alcohol increases membrane fluidity, a condition that leads to an adaptive change in the phospholipid composition of the membranes, with resultant greater rigidity of the membranes. The effects of alcohol on the lipid bilayer of the plasma membrane, when combined with other nonspecific insults, may lead to a drastic increase in calcium permeability; the resulting calcium influx may cause cell necrosis and initiate irreversibly cardiomyopathy. It is likely that changes in membrane fluidity also exert profound effects on enzyme and transport activities of membrane-bound proteins. In addition, alcohol may interact directly with the hydrophobic regions of proteins. Such interactions may play an important role not only in membrane-bound proteins, but also in alcohol-induced changes in contractile proteins of the heart. It is suggested that, in general, the effects of alcohol are similar to those of other anesthetic agents, and that the elucidation of the pathogenesis of alcoholic cardiomyopathy may require a deeper understanding of the physical interaction among alcohol, phospholipids, and proteins.