Two different conditions responsible for cardiac hypertrophy in the rat were investigated: the first one is isoproterenol-induced myocardial infarct, the second is 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: evaluation of dry heart weight value, concentration of radiothallium (201T1) in the heart and effects of inhibitors of protein synthesis (Puromycin). Experimental results have showed: (A) a significant increase (p<0.001 as compared to control group) of dry heart weight values both in isoproterenol-treated and hypoxic rats; (B) a significant increase over control group (p<0.001) in myocardial 201T1 concentration in isoproterenol-treated rats; (C) total inhibition of cardiac hypertrophy in Puromycin treated group subjected to hypoxia. Finally, on the basis of different mortality observed in infarcted (85.0%) or hypoxic (5.0%) rats treated with Puromycin (40 mg/Kg body weight 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 is only due to increased cardiac work.