CA2+ TRANSIENTS AND CELL SHORTENING IN DIABETIC RAT VENTRICULAR MYOCYTES

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.