The inhibiting effect of a plasma globulin on arterial thrombus formation, (as compared to dipyridamole).

The 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(l)], the maximal thrombus value [m(T)], the maximal thickness of the thrombus [m(D)] and the maximal thrombus surface [m(O)].

A standardized 'in vivo' model for the study of experimental arterial thrombosis: description of a method.

A method for "in vivo" induction and registration of arterial platelet thrombosis has been developed and standardized in a branch of the mesenteric artery of the white Wistar rat. It consists in local deendothelialization by electrical current. Thrombus induction is performed by topical superfusion with ADP; when the superfusion is discontinued the thrombus disappears but can again be induced reproducibly by renewal of the ADP superfusion after a time interval not exceeding 15 minutes. Registration of the thrombotic phenomenon is made possible by microprojection of the investigated arterial segment. An appropriate optoelectronic device allows the on-line derivation of discriminating parameters. Off-line storage and processing of the experimental data by computer is provided. The method is automatized and can easily be applied to other species of laboratory animals.

[Effect of an enzyme, thrombic type, defibrase, on the formation of the white intra-arterial thrombus]. / Effet d'une enzyme du type thrombique, la défibrase, sur la formation du thrombus blanc intra-artériel

The effect of intravenously administered defibrase was studied on the white intra-arterial thrombus. The administration resulted in all experimented animals in a statistically significant decrease of the thrombus formation.

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.

Role of prostaglandin biochemical pathway in platelet-vessel wall interaction and local thrombosis.

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 adenosine 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.