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Severe myocardial necrosis was produced in virgin Sprague-Dawley rats without preexisting arteriosclerosis and in breeder Sprague-Dawley rats with various degrees of arteriosclerosis by giving two subcutaneous injections of isoproterenol; the virgin rats received 50 mg/100 g and the breeder rats 25 mg/100 g body weight. Breeder rats withstood the stress and shock of myocardial necrosis with fewer untoward effects than the virgin animals. Changes in the thymus and adrenal glands also indicated that the arteriosclerotic breeder rats responded with a different pattern of adrenocortical activity. There were marked differences between the nonarteriosclerotic and arteriosclerotic rats in the fluctuation of serum transaminases and lactic dehydrogenase levels during the stress of myocardial necrosis. During the acute stages of myocardial necrosis there was intense activation of lipid metabolism with gross and microscopic evidence of intense fatty infiltration of the liver; during myocardial repair this lipid was removed concomitantly with reduction of hypercholesteremia. The dichotomy of response has been ascribed to the possibility that the preexisting arteriosclerosis in the breeder rats led to the development of increased collateral coronary artery circulation which afforded some degree of protection to the myocardium.

Responses to Drug-Induced Myocardial Necrosis in Rats with Various Degrees of Arteriosclerosis