Prostacyclin (PGI2) has been reported to be a labile but potent inhibitor of platelet aggregation and a powerful vasodilator. This paper reports the effect of trapidil on PGI2 generation in rat aorta by means of bioassay system. The aortic ring was incubated in 0.05 M Tris HCl buffer (pH 7.5) for 10 min. This incubation medium was added into human PRP, and then incubated at 37 degrees C for 2 min., and ADP was added. PGI2 activity was assayed by the inhibitory percentage of ADP induced platelet aggregation. When the aortic ring was incubated in a medium containing trapidil, PGI2 generation was accelerated. This acceleration was inhibited by pretreatment with indomethacin. Moreover, the aortas of rats intravenously injected with 30 mg/kg of trapidil were incubated in the same way, and PGI2 activity in the medium was estimated. More potent PGI2 activity was observed in the aortas of rat treated with trapidil compared with the controls. These results indicate that acceleration of PGI2 generation from aorta by trapidil is involved in the mode of action of this drug of thrombus formation.