Effect of insulin treatment on prostacyclin in experimental diabetes.

Diabetic patients have a high susceptibility to microvascular complications, atherosclerosis and thrombosis. Platelet hyperreactivity possibly related to an imbalance in arachidonic acid metabolism may be involved. Aortic rings or renal cortex produced a potent inhibitor of platelet aggregation, identified as prostacyclin (PGI2). Release of PGI2 by tissues from streptozotocin -- diabetic rats (aorta: 0.07 +/ 0.1 ng/mg wet weight; renal cortex 0.004 +/- 0.001 ng/mg wet weight) was significantly depressed when compared with controls (aorta: 0.26 +/- 0.07 ng/mg wet weight; renal cortex: 0.009 +/- 0.001 ng/mg wet weight). Treatment of diabetic animals with insulin for 8 days restored PGI2 production to normal. The finding that PGI2 is depressed in the aorta and in the kidney, tissues which develop angiopathy, and that this is normalised by insulin, suggests that impaired PGI2 production, perhaps associated with platelet hyperreactivity may play a role in the vascular complications of diabetes.