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Prostacyclin is considered to play an important role for the prevention of thrombosis due to its potent inhibition of platelet function. In this report the effect of platelet aggregating agents on prostacyclin generation from aorta and arterial microsome was investigated. Prostacyclin activity was estimated by the inhibition percentage of ADP induced platelet aggregation.Thrombin (5×10-2-5×10-5U/ml) and collagen (5×10-7-5×10-9g/ml) accelerated the prostacyclin generation from rat aorta. The effect of these agents was disappeared by the addition of indomethacin. Epinephrine did not have any influence on prostacyclin generation. Next, arterial microsome was incubated with PGH2 in various concentrations of thrombin or collagen for 2min. at room temperature. The addition of these agents potentiated prostacyclin activity in this system.These results indicated that the contact of endotherial cells with thrombin or collagen would induce the release of prostacyclin from arterial wall. This phenomenon may be one of the defense mechanisms for platelet aggregation which induce thrombosis.

Effect of platelet aggregating agents on prostacyclin generation from arterial wall