Abstract
This study was undertaken to elucidate the effect of pressure load on the development of cardiomyopathy induced by daunorubicin in the right ventricle of rabbits on which pulmonary stenosis had been performed. The right ventricular pressure after occlusion of the pulmonary artery was approximately twice that prior to occlusion. Pulmonary stenosis apparently produced hypertrophy of the right ventricular myocardium within approximately 2 weeks of occlusion. In rabbits with pulmonary stenosis, the characteristic myocardial degenerative changes induced by daunorubicin were found on the right ventricular wall. However, in rabbits without pulmonary stenosis, myocardial lesions were observed only on the left ventricular wall. The pressure load acting as a mechanical stress increases myocardial damage induced by daunorubicin. It is well known that anthracyclines take effect on cells in which nucleic acid synthesis is augmented and the pressure load results in the enhancement of protooncogene expression in myocytes and a subsequent increase in protein synthesis. These results suggest that the pressure load may play a significant role in anthracycline cardiomyopathy by increasing protein synthesis in the myocardium.
Published Version
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