Key result
Inhibition of PGI2 synthetase increases adenosine diphosphate-induced platelet thrombosis, suggesting the ratio of cyclic endoperoxides to prostacyclin triggers local thrombosis.
The balance between cyclic endoperoxides and prostacyclin is a key determinant of platelet-vessel wall interaction and local thrombosis.
Animal data on PGI2 balance in thrombosis are hypothesis-generating; human studies needed before any clinical consideration.
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.
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Bourgain et al. (2009) conducted a review in Platelet-vessel wall interaction and local thrombosis. Inhibition of PGI2 synthetase was evaluated on Platelet thrombosis. Inhibition of PGI2 synthetase increases adenosine diphosphate-induced platelet thrombosis, suggesting the ratio of cyclic endoperoxides to prostacyclin triggers local thrombosis.
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