Abstract The intact vascular endothelial surface is considered to be ‘non-thrombogenic’, and blood platelets usually fail to adhere to it. In this role, the endothelium serves to maintain the integrity of the vascular system by preventing the escape of blood and by preventing the build-up of solid thrombus within the vessel, which would compromise blood flow. A possible explanation for the non-thrombogenic effect of the endothelium is the presence of prostacyclin (PGI2), the potent inhibitor of platelet aggregation and adherence, which is produced and released by the endothelium in response to various stimuli. Removal of PGI2 from the endothelium by four different methods did not increase baseline platelet adherence, but did increase thrombininduced platelet adherence from 4 to 60%. Addition of exogenous PGI2, at low concentrations reversed the enhanced thrombin-induced platelet adherence under these conditions. Although it is unlikely that prostacyclin is the sole factor regulating platelet adherence to the endothelium, it appears to play a major role in the interaction of platelets with components of the blood vessel wall.