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Jpn Circ J. 1993 May;57(5):449-57.

Ca2+ transients and cell shortening in diabetic rat ventricular myocytes.

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Third Department of Internal Medicine, Hamamatsu University School of Medicine, Japan.


To investigate the role of abnormal Ca2+ metabolism in the diminished contractile function of diabetic myocardium, we measured the Ca2+ transients and cell contraction of diabetic rat myocytes. Isolated diabetic (8 weeks after 40 mg/kg streptozotocin, i.v.) and normal myocytes were loaded with acetoxymethyl ester of indo-1 (indo-1/AM). Ca2+ transients and cell circumferential shortening were measured simultaneously, using high temporal resolution video image analysis. The diastolic base and systolic peak of Ca2+ transients were significantly lower in diabetic myocytes than in normal myocytes (peak ratios: 0.49 +/- 0.02 vs 0.56 +/- 0.01, p < 0.05; base ratios: 0.43 +/- 0.01 vs 0.48 +/- 0.01, p < 0.01, Mean +/- SE). The cell circumferential shortening of diabetic myocytes was also significantly lower than that of normal myocytes (2.9 +/- 0.3% vs 5.2 +/- 0.9%, p < 0.05). Although isoproterenol (10(-8) and 10(-7) M) increased the peak of Ca2+ transients in both diabetic and normal myocytes, the peak value of Ca2+ transients in the diabetic group was significantly lower than that in the normal group. The decreased Ca2+ transients may be responsible for the decreased contractile function in diabetic myocardium.

[Indexed for MEDLINE]

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