Myocardial hypertrophy in the rat. Correlation between two experimental models.
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.
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology* / Q000378:metabolism; D004195:Disease Models, Animal; D006321:Heart / Q000033:anatomy & histology; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism; D007545:Isoproterenol; D008297:Male; D009203:Myocardial Infarction / Q000139:chemically induced / Q000150:complications; D009206:Myocardium / Q000378:metabolism; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology; D051381:Rats
D011691:Puromycin; D007545:Isoproterenol