Role of the vascular endothelium.

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 did not increase baseline platelet adherence, but did increase thrombin-induced platelet adherence from 4 to 60%. Additions 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. Conditions which predispose to adherence of platelets to the vessel wall may involve entrapment of tumor cells and lead to metastasis formation. Whether prostacyclin and other factors involved in the non-thrombogenic character of the vascular endothelium provide a significant defense against attachment of tumor cells is not known, but the potential for such a primary or secondary role clearly exists. In our studies, prostacyclin did not appear to influence the adherence of Raji lymphoma cells to the endothelium. Additional studies are indicated to correlate adherence of tumor cells to the vascular wall with their potential for formation of metastatic lesions.