No abstract

Prostaglandins play an important role in the platelet-vessel wall interaction. The inhibition of PGI2 synthetase results in an increase of platelet thrombosis induced by adeno-sine diphosphate. Addition of exogenous arachidonic acid further increases the phenomenon. The ratio of cyclic endoperoxides (PGG₂ and PGH₂) to prostacyclin (PGI₂) could well be the determining trigger in platelet-vessel wall interaction and local thrombosis.

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.

SummaryThe inhibiting effect on arterial white thrombus formation of a globulin prepared from beef plasma has been compared to dipyridamole in white Wistar rats. It was demonstrated that the globulin fraction had a greater effect in inhibiting thrombus formation as judged by the lag time [t(1)], the maximal thrombus value [m(T)], the maximal thickness of the thrombus [m(D)] and the maximal thrombus surface [m(O)].