In an in vivo model developed for the study of arterial thrombosis in the white Wistarrat, it was demonstrated that superfusion of the investigated arterial segment with cyclo oxygenase inhibitors (ASA, indomethacin, flurbiprofen) resulted in a marked decrease of ADP-induced thrombosis while tranylcypromine enhanced the thrombotic phenomenon. As other MAO inhibitors were without effect, it was concluded that tranylcypromine possibly decrsibsed the PGE2-synthetase activity of the vessel wall. In the light of these findings we then suggested that the platel et-vessel wall interaction was dependent at least to some extent on the cyclic endoperoxides-PGI2 ratio of the endothelium and eventually of the deeper vascular structures. Electron microscopic studies on arterial segments used in our model revealed that suloctidil markedly decreases smooth muscle cell hypertrophy following local deendothelialization. Furthermore reconstitution of the endothelial lining consisting in endothelial cell hypertrophy and sliding over the dcendothelialized are until cell contact is made was also delayed. Following the intravenous administration of suloctidil (0.5 mg/kg) in our model the thrombus enhancing effect of locally superfused tranylcypromine was Offset. These experiments suggest that a decreased PGI2-synthetase activity is inhibited by a platelet function active drug such as suloctidil.
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