Sarcolemmal Alterations during Catecholamine Induced Cardiomyopathy

Abstract

Circulating levels of catecholamines are increased dramatically under stressful conditions and these hormones are generally considered responsible for the development of stress-associated cardiomyopathy. In fact varying degrees of ultrastructural abnormalities as well as cellular necrosis have been shown to occur in the myocardium upon injecting animals with large doses of catecholamines including isoproterenol (1,2,3). Although earlier studies have demonstrated the occurrence of intracellular Ca²⁺ overload during the development of catecholamine-induced necrosis (4,5,6), the exact mechanisms for its pathogenesis are poorly understood. Since catecholamines are known to activate the β-adrenergic receptor-adenylate cyclase system and thereby increase calcium influx, it is generally assumed that the occurrence of intracellular Ca²⁺ overload due to high levels of circulating catecholamine is a consequence of massive Ca²⁺ entry through calcium channels in heart sarcolemma. Previous studies have indicated that other membrane systems such as sarcoplasmic reticulum and mitochondria, which are also known to regulate the cytoplasmic concentration of Ca²⁺, also are affected during the occurrence of catecholamine-induced cardiomyopathy (3,7,8).

This research was supported by a grant from the Manitoba Heart Foundation.

Dr. V. Panagia was the Murphy Foundation Scholar.