1982
DOI: 10.1159/000214653
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Role of the Prostaglandin Biochemical Pathway in Platelet-Vessel Wall Interaction and Local Thrombosis

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.

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Cited by 3 publications
(3 citation statements)
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References 9 publications
(15 reference statements)
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“…Exogenous PGI2 can partially inhibit the binding of platelets to newly exposed areas of the subendothelium (1,3,27,28). There is, however, conflicting data concerning whether inhibition, of vascular PGI2 production by nonsteroidal antiinflammatory agents enhances platelet adherence to newly deendothelialized areas of arterial walls (29)(30)(31)(32). Nevertheless, after a damaged artery begins to repair itself, there is an increase in the capacity bf the deendothelialized vessel to form PGI2 from arachidonic acid that correlates with the formation of a nonthrombogenic neointimal surface (26).…”
Section: Discussionmentioning
confidence: 99%
“…Exogenous PGI2 can partially inhibit the binding of platelets to newly exposed areas of the subendothelium (1,3,27,28). There is, however, conflicting data concerning whether inhibition, of vascular PGI2 production by nonsteroidal antiinflammatory agents enhances platelet adherence to newly deendothelialized areas of arterial walls (29)(30)(31)(32). Nevertheless, after a damaged artery begins to repair itself, there is an increase in the capacity bf the deendothelialized vessel to form PGI2 from arachidonic acid that correlates with the formation of a nonthrombogenic neointimal surface (26).…”
Section: Discussionmentioning
confidence: 99%
“…The participation of platelet cyclooxygen ase activity in this type of experiments can indeed be excluded [5], Our working hypoth esis is that the trigger for adhesion and aggre gation of platelets onto the intimal structures is geared by the ratio of the cyclic endoperoxides to prostacyclin within the arterial wall. An increase in the value of the ratio enhances the thrombotic phenomenon, while a de crease induces the opposite.…”
Section: Introductionmentioning
confidence: 97%
“…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.…”
Section: Introductionmentioning
confidence: 99%