The Role of Cyclooxygenase in Arterial Platelet Vessel Wall Interaction

Coronary Vasoconstrictor and Vasodilator Actions of Arachidonic Acid in the Isolated Perfused Heart of the Rat

“…The TxA2-like synthetase could be selectively inhibited by Dpy, Spyz or low concentrations of ASA. These data do not preclude the importance of platelet synthesized TxA2 acting as a pro-aggregatory factor involved, for instance, in vascular injuries (Srivastava, 1978;Gorman, 1979;Bourgain, Andries & Finne, 1979). However, the vascular synthesis of TxA2 may further aggravate the compromised coronary flow by inducing vasoconstriction.…”

Role of the Prostaglandin Biochemical Pathway in Platelet-Vessel Wall Interaction and Local Thrombosis

“…It was demonstrated in previous publications that T [3] and 15-hydroperoxyarachidonic acid [4], both inhibitors of the PGI2 synthetase, markedly enhanced thrombosis while the in hibitors of the cyclooxygenase [1,2] activity with compounds such as ASA, indomethacin [1] or flurbiprofen [2] significantly decreased locally induced platelet thrombosis. These results suggested that one of the determining factors in the generation of thrombus forma tion could well be the ratio of PGG2-PGH2 to Table I T AA + T T AA + T T AA + T T AA + T 1 44 31 44 60 230 210 10 8 70 70 2 16 11 54 64 570 875 9 8 185 280 3 11 19 81 94 163 255 5 7 55 70 4 25 18 61 78 300 375 5 8 162 125 5 27 18 64 93 210 407 10 11 90 139 6 20 13 80 89 580 527 10 8 1,033 1,...…”

“…In previous investigations the role of the prostaglandin biochemical pathway in the generation of white platelet thrombosis was clearly established [1][2][3][4], Evidence was ad duced that the adhesion of platelets onto the intimal structures followed by thrombus for mation was determined mainly by the ratio of the cyclic endoperoxides (PGG2-PGH2) to prostacyclin (PGI2) present in the vessel wall.…”

Effect of Cyclooxygenase Inhibition on Platelet-Vessel Wall Interaction

“…In previous investigations the role of the prostaglandin biochemical pathway in the generation of an arterial white platelet thrombus was clearly established [1][2][3][4][5]. Ex perimental evidence was adduced that fol lowing the stimulation of platelet function by adenosine diphosphate (ADP) the adhesion of platelets onto the vessel wall followed by aggregation and thrombosis could well de pend on the ratio of cyclic endoperoxides to prostacyclin generated in the endothelial cells.…”

“…These phenomena are evidenced by elec tronically processed microprojection [6] and ultrastructural control [7], Topical superfusion with inhibitors of cy clooxygenase such as acetylsalicylic acid (ASA), indomethacin, and flurbiprofen [1,2] results in an immediate and statistically sig nificant decrease of the ADP-induced throm botic phenomenon; conversely, superfusion with inhibitors of PGI2 synthetase such as tranylcypromine [3] and 15-hydroperoxyara-chidonic acid [4] markedly enhances throm bosis. These compounds interfere with the prostaglandin metabolism of the cells of the vessel wall, evidently also those surrounding the small area of desendothelialization.…”