P-selectin (PADGEM protein, GMP-140 or CD 62) is a glycoprotein of platelet a-granules and endothelial Weibel-Palade bodies that, by mediating cellular adhesion, initiates recruitment of leukocytes and lymphocytes into injured tissue. Both of the endothelial antiplatelet autacoids prostacyclin (PGI2) and nitric oxide (NO) have been demonstrated to inhibit P-selectin expression. Prostaglandin endoperoxides PGG2/PGH2that are generated by activated platelets have been demonstrated to be used by endothelium for generation of prostacyclin. In an experimental modelin vitrothat resembles vessel wall/platelet/PMN interactionin vivo, we found that aspirin (100μM), a COX inhibitor, but not L-NMMA (100μM) and a NO-synthase inhibitor, reversed the inhibitory effect of arterial wall on P-selectin mediated platelet/PMN adhesion. The anti-adhesive potency of vessel wall reversed by aspirin was dose-dependently restored by camonagrel (3-100μM), a new TXA2synthase inhibitor. We conclude that selective TXA2-synthase inhibitors may inhibit P-selectin mediated platelet/PMN adhesion by augmenting formation of prostacyclin by vessel walls.