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

S. W. Schaffer, Mahmood S Mozaffari, M. Artman, G. L. Wilson

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Abstract

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 μM, the rates of sarcoplasmic reticular calcium uptake and adenosinetriphosphatase activity of the diabetic hearts were decreased ~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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume256
Issue number1
Publication statusPublished - Jan 1 1989
Externally publishedYes

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ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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