Abstract
The factors affecting PGI2 synthesis following the platelet aggregation induced by collagen (1μg/ml) in whole blood were examined.Trapidil, possessing the anti-platelet aggregating activity and the enhancing effect of PGI2 synthesis in endothelial cells, markedly promoted PGI2 synthesis in whole blood, while aspirin showed no effect. The increment of PGI2 synthesis ran parallel to the concentration of trapidil, whereas TxA2 synthesis was decreased. OKY-046, the inhibitor of TxA2 synthetase, also increased PGI2 level and decreased TxA2 level in whole blood in the same manner of trapidil. The level of PGI2 in the suspension of leukocytes added trapidil (1mM), arachidonic acid (0.3M) and collagen (1μg/ml) was signficantly higher than that in the suspension added 1mM of aspirin in place of trapidil.These results suggest that trapidil has the inhibitory activity of TxA2 synthetase, resulting in the increment of PGI2 in whole blood. This synthesis of PGI2 was found in the leukocyte suspension in the presence of arachidonic acid.
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