Abstract
Prostacyclin (PGI2) mainly produced from vascular walls has an inhibitory effect on platelet aggregation. It has been reported that, in diabetes mellitus, PGI2 production is decreased and platelet thromboxane B2 (TXB2: a stable metabolite of thromboxane A2) production is increased, leading to vascular complications. In this study, the relationship between plasma 6-keto-prostaglandin F1α (6 KF: a stable metabolite of PGI2) level and platelet function in diabetes mellitus was examined.
Plasma 6 KF level was significantly decreased in diabetics with proliferative retinopathy (DP) compared with age-matched controls (247.1±41.8 vs. 378.4±45.5pg/ml). On the other hand, platelet aggregation rate (78±4%) and TXB2 production during aggregation (8.34±1.70 nmol/1010 platelets) were significantly increased in DP compared with controls (37±9, 2.60±0.56), respectively. It was observed that plasma 6 KF level was significantly inversely correlated with platelet aggregation rate and TXB2 production during aggregation. On the other hand, samples of aorta obtained from streptozotocin-induced diabetic rats produced less PGI2-like substance than samples from controls.
These results suggest that decreased plasma PGI2, which would be derived from decreased aortic production, may be one of the causes of abnormal platelet function in diabetes mellitus.
