The hemostatic response to endothelial damage is contingent upon the coordinated interaction between platelets and vessel wall constituents. Under basal conditions, platelets circulate in the resting state and are not avid for the endothelium. The endothelium further maintains this non-thrombogenic milieu by synthesizing cell products and expressing surface molecules that inhibit platelet activation. Endothelial cells metabolize endoperoxides to prostacyclin, which inhibits platelet aggregation by activating platelet adenylyl cyclase and augmenting levels of cAMP (Leopold and Loscalzo, 1995). The nitrosovasodilators, endothelium-derived-relaxing factor and nitric oxide, diffuse through platelet membranes to increase cGMP levels and, thereby, prevent platelet adhesion (Leopold and Loscalzo, 1995). Endothelin additionally enhances these mechanisms by stimulating prostacyclin synthetase and nitric oxide synthase (Thiemermann et al., 1988; Herman et al., 1989; Lidbury et al., 1990). Endothelial cells constitutively express thrombomodulin, a surface receptor which binds thrombin with high affinity and facilitates the protease’s activation of protein C; and the enzyme ectoADPase, which converts ADP to AMP (Leopold and Loscalzo, 1995). Endothelial cell dysfunction perturbs these homeostatic mechanisms and promotes platelet adhesion and activation.