Potential Oxidative Pathways of Catecholamines in the Formation of Lipid Peroxides and Genesis of Heart Disease

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Abstract
Results of clinical and experimental animal studies have shown that unusually high levels of catecholamines in the blood cause a variety of morphological and functional changes in the heart (1, 18, 22, 25, 28). The endogenous stores of adenine triphosphate and creatine phosphate are depleted (8, 25, 26) and mitochondrial structure-function is impaired (7, 15). Intracellular increase in calcium has been considered to be a determinant factor in this as well as in variety of other models of heart cell damage (8, 21). In this regard catecholamine-induced cardiomyopathy, has been shown to be accompanied by a significant increase in the myocardial calcium content (8,15) indicating changes in the membrane permeability. Strong evidence for the alterations in the permeability of sarcolemma due to isoproterenol treatment was provided by the intracellular diffusion of horseradish peroxidase, an extracellular protein tracer, following the drug injection (19).