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Interaction of platelet and vessel wall is one of the most important problems on the development of thrombotic disorder, and from the aspect of arachidonic acid metabolism, whether the platelet PG endoperoxides may be utilized as a substrate for PGI2 biosynthesis in vessel wall has been a point of discussion. This paper reports the possible mechanism of conversion of platelet PG endoperoxides to PGI2 synthesis in cyclo-oxygenase inhibited aortic ring. Aortic ring and Acetyl Salicylic Acid (ASA)-treated aortic ring were incubated with plateletpoor plasma (PPP), platelet-rich plasma (PRP), or OKY-1581, a thromboxane A2 (TXA2) synthetase inhibitor, treated PRP. TXA2 and PGI2 were measured by RIA as TXB2 and 6-keto-PGF1α respectively. There was no increase of PGI2 synthesis in the intact aortic ring, when the platelet TXA2 synthesis was inhibited by OKY, however the increased PGI2 synthesis was observed in ASA-treated aortic ring. Marked increase of PGI2 synthesis was observed in ASA-treated aortic ring with the existence of OKY-treated PRP. Arterial microsome also significantly increased PGI2 synthesis in OKY-treated PRP comparing with PPP or PRP. When ASA-treated aortic ring was incubated with PGH2, PGI2 synthesis was significantly increased, while there was a little PGI2 synthesis, when it was incubated without PGH2 as control. These results indicate the possible salvage pathway for PGI2 synthesis from PG endoperoxides of the platelet in cyclo-oxygenase inhibited aortic ring.
- 一般社団法人 日本血栓止血学会の論文
一般社団法人 日本血栓止血学会 | 論文
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