The action of cyclooxygenase and prostacyclin-synthetase inhibitors on platelet-vessel wall interaction.

PGG2 and PGH2 are present both in the arterial wall and the platelets, in the platelet thromboxane A2 is generated while in the endothelium PGI2 is synthetized. In an "in vivo" model we demonstrated that topical superfusion of the arterial segment with ASA, indomethacin or flurbiprofen results in a marked decrease of local white platelet thrombus formation while superfusion with PGI2 synthetase inhibitors results in thrombus enhancement. This demonstrates that the adhesion of platelets onto the vessel wall and subsequent aggregation depend among other possible mechanisms on the ratio PGG2-PGH2 versus PGI2.