Disturbances of the heart structure and function in chronic hemolytic anemia, their compensation with increased coronary flow, and their prevention with ionol, an inhibitor of lipid peroxidation.

The structure and function of heart muscle were studied in rats with chronic hemolytic anemia induced by phenylhydrazine. Contractural lesions, myocytolysis, fatty dystrophy, and small-focal necrosis were found in the myocardium along with hypertrophy. The disturbances were accompanied by a compensatory increase in the coronary flow by 2.5-fold during myocardial contractions. When the coronary flow of isolated hearts was experimentally decreased to the control level, a great depression of the contractile function developed. Administration of the antioxidant ionol, an inhibitor of lipid peroxidation, simultaneously with phenylhydrazine did not prevent the development of the hemolytic anemia, but decreased by 2 times the degree of hypertrophy and the amount of the lesion foci in the heart muscle. It also significantly inhibited the compensatory increase of coronary flow and completely eliminated depression of the heart contractile function during the normalization of coronary flow. The data allow a suggestion that hemolytic anemia is accompanied by activated lipid peroxidation, this process playing a role in the myocardial damage of anemia. Antioxidants can prevent such damage.