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.

F Z Meerson, M E Evsevieva
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引用次数: 7

Abstract

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.

慢性溶血性贫血的心脏结构和功能紊乱,冠状动脉血流增加对它们的补偿,以及脂质过氧化抑制剂离子醇的预防。
研究了苯肼致慢性溶血性贫血大鼠心肌的结构和功能。收缩性病变、肌细胞溶解、脂肪营养不良、小局灶性坏死伴心肌肥大。在心肌收缩期间,这些紊乱伴随着冠状动脉血流代偿性增加2.5倍。当离体心脏的冠状动脉血流实验降低到控制水平时,收缩功能明显下降。同时给予抗氧化剂离子醇(一种脂质过氧化抑制剂)和苯肼并不能预防溶血性贫血的发生,但能使心肌肥厚程度和病灶数量减少2倍。显著抑制冠状动脉血流代偿性增加,完全消除冠状动脉血流正常化过程中对心脏收缩功能的抑制。这些数据表明,溶血性贫血伴随着活化的脂质过氧化,这一过程在贫血的心肌损伤中起作用。抗氧化剂可以防止这种损害。
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