Abstract
Catecholamines in large doses are known to produce cardiac hypertrophy (1,2,3) as well as myopathic changes (2,4). The necrotic lesions observed have been compared to those seen in ischemic heart disease (5). Several factors including intracellular calcium overload and exhaustion of high energy phosphates (6), free radical production (7) and an increase in cAMP levels (8) have been proposed to explain this catecholamine-induced necrosis; however, the exact mechanisms involved in this condition are far from clear. There is strong evidence that in many tissues lysosomes play an important role in the turnover of tissue proteins and other macromolecules (9,10,11). Alterations in lysosomal enzymes have been reported in certain types of cardiomyopathy (12,13,14) and cardiac ischemia (15,16) where hydrolytic degradation of subcellular components by lysosomal enzymes has been implicated in the pathogenesis of cell injury. It is generally believed that isoproterenol-induced cardiomyopathy in rats forms a good model for studying the pathogenesis of myocardial changes under stressful conditions. In this report, therefore, we have examined the alterations in some lysosomal enzyme activities in the rat myocardium within 24 hours of catecholamine injection in order to test if such changes are associated with the development of catecholamine-induced cardiomyopathy.
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© 1985 Martinus Nijhoff Publishing, Boston
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Roman, S., Kutryk, M.J.B., Beamish, R.E., Dhalla, N.S. (1985). Lysosomal Changes during the Development of Catecholamine-Induced Cardiomyopathy. In: Beamish, R.E., Panagia, V., Dhalla, N.S. (eds) Pathogenesis of Stress-Induced Heart Disease. Developments in Cardiovascular Medicine, vol 46. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2589-5_23
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DOI: https://doi.org/10.1007/978-1-4613-2589-5_23
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