Steroids Produced in Vitro by Adrenal Glands of Normal and Arteriosclerotic Rats During and After Drug-Induced Myocardial Necrosis

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Abstract
The subcutaneous injection of the potent catecholamine, isoproterenol, on two consecutive days causes active and massive myocardial necrosis in rats. Infarctoid myocardial necrosis was produced in male and female virgin rats free of arterial disease, in male breeder rats which have microscopic arteriosclerosis only, and in female breeder rats having early or advanced gross arteriosclerosis. During the active development of myocardial necrosis and heart failure, an apparent shift in distribution of body fluid produced systemic dehydration, pulmonary edema, and hydrothorax. Animals which survived the myocardial destruction showed gradual reduction of the congestive heart failure and beginning myocardial repair. Virgin animals with no pre-existing arterial disease developed more severe signs of shock and congestive heart failure than breeder rats with pre-existing arteriosclerosis. In vitro estimation of the adrenal steroids produced by the animals with myocardial necrosis indicated intense in vivo stimulation of adrenocorticoid production coincident with the increasing severity of the myocardial necrosis. Steroid production returned to normal during progressive myocardial repair. Virgin rats showed a very prompt adrenal response to the stress of myocardial destruction but breeder rats, which also have pre-existing reduced adrenal function, showed a lag in the response of their adrenal glands. Chemical and histological analyses of the adrenal glands indicated a pronounced increase of aldoster-one production during the experiment, this increase being associated with loss of fluid and electrolytes from the vascular space. The production of aldosterone appears to be vital to the physiological adjustments needed by these animals during heart failure because the production of aldosterone seems to occur at the expense of the other adrenal steroids, e.g., corticosterone, 18-hydroxy-deoxycorticoster-one and total steroid. These comparative studies suggest that adrenal responsiveness during the stress of myocardial infarctoid necrosis is quantitatively different in animals free of previous arterial disease from that found in animals with pre-existing microscopic or grossly visible arteriosclerosis. The specific kind and the amount of adrenal steroid produced during myocardial destruction may be of vital importance for survival.