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.