Key result
Induction of cardiac hypertrophy in rabbits via isoprenaline (5 days) or thyroxine (15 days) was accompanied by myocardial cell necrosis, altered enzyme ratios, and morphological changes.
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Hypothesis-generating for necrosis during hypertrophy; clinical relevance in humans remains undetermined.
Cardiac hypertrophy was induced in rabbits by injecting thyroxine or isoprenaline, or by surgically constricting the abdominal aorta. An increase in heart weight was associated with a change in the ratios of bound to free forms of five lysosomal enzymes, a change in serum creatine phosphokinase and lactate dehydrogenase, and a change in the morphology of the myocardial cells. Isoprenaline treatment for 5 days induced a maximal change in heart weight, in the ratio of lysosomal enzymes, and in the serum enzymes. Thyroxine treatment was required for 15 days before maximal changes in heart weight, ratio, and serum enzymes were observed. In contrast, coarctation of the aorta caused a progressive change in heart weight, in the ratio of lysosomal enzymes, and in serum enzymes. These results suggest that necrosis of the myocardial cells does indeed accompany cardiac hypertrophy. It was further observed that autophagosomes, degenerating mitochondria in the myocardial cells during the induction of cardiac hypertrophy, and myofibril lysis were found, all of which confirms the suggestion of myocardial cell necrosis in the experimentally enlarged heart.
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Revis et al. (1979) studied Cardiac hypertrophy. Thyroxine, isoprenaline, or surgical constriction of the abdominal aorta was evaluated on Myocardial cell necrosis, heart weight, lysosomal enzyme ratios, and serum enzymes. Induction of cardiac hypertrophy in rabbits via isoprenaline (5 days) or thyroxine (15 days) was accompanied by myocardial cell necrosis, altered enzyme ratios, and morphological changes.
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