AJP - Endocrinology and Metabolism, Vol 256, Issue 1 E25-E30, Copyright © 1989 by American Physiological Society

ARTICLES

Basis for myocardial mechanical defects associated with non-insulin-dependent diabetes

S. W. Schaffer, M. S. Mozaffari, M. Artman and G. L. Wilson
Department of Pharmacology, University of South Alabama School of Medicine, Mobile 36688.

Hearts isolated from 12-mo non-insulin-dependent diabetic rats exhibited reduced rates of contractility and relaxation. Associated with the abnormality in contractility was a redistribution in myosin isozyme content to the least active V3 form. Defects in myocardial relaxation also occurred concomitantly with impaired handling of calcium. Total tissue calcium content rose 35% in the diabetic hearts. At the same time, the activity of the pump responsible for maintaining normal cytoplasmic calcium levels was reduced. At a free calcium concentration of 2.0 microM, the rates of sarcoplasmic reticular calcium uptake and adenosinetriphosphatase activity of the diabetic hearts were decreased approximately 30%. Diastolic ventricular stiffness increased dramatically. The net result of these abnormalities in calcium metabolism is a significant impairment in mechanical performance of the diabetic heart.

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