[Myocardial ultrastructure, energetics and function in chronic adriamycin-induced lesions].

V I Kapel'ko, M I Popovich, V G Sharov, S I Kostin, M A Golikov
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Abstract

The ultrastructural study of the myocardium of rats received adriamycin for 8-10 weeks revealed the picture of mosaic lesions of cardiomyocytes. Cells with little changes were coincided with apparently changed cardiomyocytes in which hypercontracted or atrophied sarcomeres with distended Z-lines, glycogen disappearance and swollen or hypertrophied mitochondria were seen. Myocardial content of ATP did not change but that of phosphocreatine was decreased by 45 percent. The pump function of the isolated heart was moderately lower that was associated with almost twofold increase in left ventricular diastolic stiffness suggesting a deterioration of its filling. A rise in Ca++ concentration in the perfusate exerted similar positive inotropic effect on hearts of both groups which was associated with a prominent fall of diastolic stiffness. Results suggest that increased diastolic stiffness in adriamycin-treated hearts may be due to both local ATP deficiency in myofibrils or incomplete Ca++ removal from them.

[慢性阿霉素诱导病变的心肌超微结构、能量学和功能]。
阿霉素给药8 ~ 10周大鼠心肌超微结构观察显示心肌细胞马赛克病变图。变化不大的细胞与变化明显的心肌细胞一致,可见肌瘤过度收缩或萎缩,z线扩张,糖原消失,线粒体肿胀或肥大。心肌ATP含量没有变化,但磷酸肌酸含量下降了45%。离体心脏的泵功能较低,这与左心室舒张刚度增加近两倍有关,表明其充盈恶化。灌注液中钙离子浓度的升高对两组心脏都有类似的正性肌力作用,这与舒张僵硬度的显著下降有关。结果表明,阿霉素处理心脏舒张硬度增加可能是由于肌原纤维局部ATP缺乏或钙离子不完全去除所致。
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