Stimulation of prostacyclin release from vessel wall by Bay g 6575, an antithrombotic compound.
Ingestion of 1.2 g Bay g 6575 daily for 1 week by six healthy volunteers had no effect on blood-coagulation, fibrinolysis, or platelet aggregation in vitro, but it seemed to inhibit platelet aggregation in vivo (shown by a smaller reduction in the platelet aggregate ratio after venous occlusion). Plasma drawn from five volunteers after ingestion of a single dose of 1.2 g of the drug stimulated prostacyclin release from slices of rat aorta which had been washed until they stopped releasing anti-aggregating substances, whereas plasma from the same individuals before ingestion of the substance did not. Administration of either Bay g 6575 or dipyridamole alone had no effect on platelet aggregation in vitro, but combined administration resulted in a striking and prolonged inhibition of A.D.P.-induced platelet aggregation. It is proposed that the previously described antithrombotic properties of Bay g 6575 in animals are due to stimulation of prostacyclin release from the vessel wall, and that this effect is also demonstrable in man.[1]References
- Stimulation of prostacyclin release from vessel wall by Bay g 6575, an antithrombotic compound. Vermylen, J., Chamone, D.A., Verstraete, M. Lancet (1979) [Pubmed]
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