Effect of aspirin on thrombin-induced adherence of platelets to cultured cells from the blood vessel wall.

An in vitro method was used to detect adherence of (51)Cr-labeled platelets to monolayers of cultured human endothelial, fibroblast, and smooth muscle cells. Washed platelets did not adhere to untreated or aspirin-treated endothelial monolayers in the absence of thrombin. In contrast, thrombin-induced platelet aggregates adhered to all of the monolayers but adherence to endothelium was significantly less than to the other cells. Additional evidence for adherence of platelets to the endothelium was provided by scanning and transmission electron microscopy. Thrombin-induced platelet adherence to endothelium was inhibited by hirudin. Platelet adherence induced by thrombin was enhanced significantly by treatment of the endothelial monolayer with 1-2 mM aspirin. This increase in adherence was seen even when aspirin-treated platelets were used; adherence values approached those seen with fibroblasts and smooth muscle cells. An aspirin concentration of 0.1 mM was sufficient to block thrombin-induced malonaldehyde production in platelets but it did not interfere with the inhibitory effect of the endothelium against platelet adherence. The effect of aspirin on the endothelium was temporary and inhibitory activity of the endothelium was restored 1 h after aspirin had been removed from the incubation system. The ability of thrombin to cause adherence of platelets to undamaged endothelium, and the potential for aspirin to enhance this adherence have implications for mechanisms which operate in platelet interaction with the blood vessel wall.