Myocardial Hypertrophy in the Rat

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Abstract
Two conditions responsible for cardiac hypertrophy in the rat were investigated: isoproterenol-induced myocardial infarct and exposure to hypoxia (0.42 atmospheres/24 h) in hypobaric chamber. To demonstrate that in both experimental models stimulation of protein synthesis is an absolute requirement to induce cardiac hypertrophy, a variety of techniques were employed including: the evaluation of dry heart weight value, concentration of 201Tl in the heart and effects of inhibitors of protein synthesis (Puromycin). Results showed the following: a significant increase (P < 0.001 as compared to the control group) of dry heart weight values both in isoproterenol-treated and hypoxic rats; a significant increase over the control group (P < 0.001) in myocardial 201Tl concentration in isoproterenol-treated rats; and total inhibition of cardiac hypertrophy in the Puromycin-treated group subjected to hypoxia. On the basis of different mortality observed in infarcted (85.0%) or hypoxic (5.0%) rats treated with Puromycin (40 mg/kg body wt i.p.), a different role of cardiac hypertrophy in 2 experimental conditions is postulated: in the case of infarct-like lesions the cardiac hypertrophy has compensatory significance; under hypoxic stimulus it is due to increased cardiac work.