Platelet Abnormalities in Experimental Diabetes

Abstract

Many abnormalities of platelet function occur in patients with diabetes mellitus, partioularly those with angiopathy. We have previously demonstrated that prostacyclin (PGI2) is decreased in streptozotocin-diabetic rats, and have now investigated platelet reactivity in these animals. Responsiveness to ADP and arachidonlc acid was increased, and platelet cyclo-oxygenase and thromboxane synthetase activities were significantly elevated (p<0.05) in diabetic animals (5.5±0.7 and 5.9±0.9 arbitrary units/109 platelets) when compared with control animals (J.0±0.4 and 3.9±0.3 arbitrary units/109 platelets). Malondialdehyde synthesis was 1,5 and 0.9 n moles per 108 platelets in diabetic and control rats respectively. Diabetic platelets were also less sensitive to the anti-aggregating effects of PGI2 (IC50: diabetic, 2.3 ng/ml; control, 1.3 ng/ml. Survival of illindium-labelled autologous platelets was significantly reduced, indicating that platelet function is abnormal in vivo, in diabetic animals. Platelet hyper-reactivity, possibly associated with depressed PGI2, could be related to the vascular complications of diabetes.