Kapel'ko V I, Saks V A, Popovich M I, Golikov M A, Veksler V I
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1987;10(1):46-52.
4-week administration of adriamycin (20 mg/kg) to rats resulted in the death of approximately one third of the animals, the minute volume of isolated hearts of the surviving animals was less than half of the normal value and the level of phosphocreatine was decreased by one third. The hearts of the rats receiving the same dose of the drug over 10 weeks maintained the same pump function and contained the same amount of macroergic phosphates as those of the control animals. In both series of experiments there was an increase of the end-diastolic pressure and the diastolic elasticity of the left ventricle. In the isovolumic regime the hearts of the rats receiving adriamycin over 10 weeks were able to develop the same pressure only if the rate of coronary blood flow was increased by approximately 1.5 times. Myofibril sensitivity to phosphocreatine deficiency in fibers with destroyed sarcolemma was decreased. The results point to considerable compensatory resources of the heart in chronic adriamycin damage to the myocardium.
给大鼠连续4周注射阿霉素（20毫克/千克）导致约三分之一的动物死亡，存活动物离体心脏的每分输出量不到正常值的一半，磷酸肌酸水平降低了三分之一。在10周内接受相同剂量药物的大鼠心脏保持相同的泵功能，并且含有与对照动物相同量的高能磷酸盐。在这两个系列的实验中，左心室舒张末期压力和舒张弹性均增加。在等容状态下，只有当冠状动脉血流量增加约1.5倍时，接受10周阿霉素治疗的大鼠心脏才能产生相同的压力。肌原纤维对肌膜破坏的纤维中磷酸肌酸缺乏的敏感性降低。结果表明，在阿霉素对心肌的慢性损伤中，心脏具有相当大的代偿能力。
