Alcoholic cardiomyopathy in mice. Myocardial glycogen, lipids and certain enzymes.

Chronic ethanol feeding to C57B1 mice for 25 weeks caused an increase in heart size, both absolutely and relative to body weight. When ethanol was fed with a diet having a methionine imbalance, the activities of acetyl CoA synthetase were depressed. Ethanol also caused functional changes in the heart mitochondria measured as a decrease in $\text{P}\text{O}$ ratios; thus it appears that alcohol per se can affect the heart. The correlation of the biochemical abnormalities in mitochondria with the ultrastructural pathology observed suggest that the C57B1 mouse may serve as a useful experimental animal model for the study of alcoholic cardiomyopathy.