To investigate the role of abnormal Ca
2+ metabolism in the diminished contractile function of diabetic myocardium, we measured the Ca
2+ 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). Ca
2+ transients and cell circumferential shortening were measured simultaneously, using high temporal resolution video image analysis. The diastolic base and systolic peak of Ca
2+ 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, Mea±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 Ca
2+ transients in both diabetic and normal myocytes, the peak value of Ca
2+ transients in the diabetic group was significantly lower than that in the normal group. The decreased Ca
2+ transients may be responsible for the decreased contractile function in diabetic myocardium.
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