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AJP - Heart and Circulatory Physiology, Vol 272, Issue 1 148-H158, Copyright © 1997 by American Physiological Society
ARTICLES |
J. Ren and A. J. Davidoff
Department of Internal Medicine, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
To determine whether diabetes-induced cardiac dysfunction is due to contractile dysfunction at the single-cell level, mechanical properties and Ca2+ transients were evaluated in ventricular myocytes isolated from diabetic rats. Rats were made diabetic by injection with streptozotocin and killed either 4-6 days or 8 wk after treatment. Shortening and relengthening (twitch) properties were evaluated in isolated myocytes with a high-resolution (120-Hz) video-based edge-detection system during electrical stimulation between 0.1 and 5 Hz. A separate cohort of myocytes was loaded with fura 2 to assess intracellular Ga2+ transients. Long-term (8-wk) but not short-term (4- to 6-day) diabetes depressed peak twitch amplitude. Diabetes markedly prolonged both the contraction and relaxation phases from both diabetic models. Additionally, 35% of the long-term diabetic myocytes could not pace at 5 Hz, and 48% of the short-term diabetic myocytes developed a hypercontracture at that frequency. Intracellular Ca2+ measurements showed slower Ca(2+)-transient decays in myocytes from short-term diabetic rats. These data demonstrate that contractile dysfunction seen in the diabetic heart is due, in part, to abnormalities of the myocyte. Furthermore, these abnormalities are present after only 4-6 days of diabetes, suggesting a rapid alteration in the processes regulating myocyte shortening and relengthening, which likely include impaired Ca2+ sequestration or extrusion.
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