Abstract
Summary
Adult, male gerbils were subjected to two sc injections of the potent beta-adrenergic stimulating agent isoproterenol. The animals promptly manifested severe tachycardia and became prostrate, and as the cardiac-stimulating effects of the drug began to wane, most of the animals began to recover. However, after the second injection of the drug, 30-40% of the animals succumbed due to shock and myocardial infarction. Myocardial necrosis, consisting of longitudinal streaks limited to the myocardium proper, became maximal on Day 3 and was no longer grossly visible by Day 8. Microscopically, scattered foci of damaged muscle cells covered with a granular admixture of calcium and mucopolysaccharide were still apparent with little or no evidence of fibroblasts or white blood cells. Concomitant with the acute myocardial ischemia, severe hepatic steatosis, islet beta cell degranulation, marked adrenal hypertrophy, and thymus gland involution, these gerbils displayed dynamic changes in circulating CPK, triglycerides, free fatty acids, cholesterol, glucose, and Cmpd. F. The changes in circulating Cmpd. F suggest that after an initial response to the duress of acute cardiac ischemia, the adrenal cortex of the gerbil is incapable of producing additional quantities of Cmpd. F. It is proposed that the pathophysiologic changes observed both in key organs and in the circulation are related to the extent and severity of the myocardium infarcted.
The author is indebted to D. Conatser, M. Springs, and E. Tryczynski for technical assistance.
Get full access to this article
View all access options for this article.