Inhibition of Prostacyclin and Platelet Thromboxane A2 after Low-Dose Aspirin

To compare the inhibitory effects of aspirin on prostaglandin synthesized by vessel walls and platelets, we obtained vein segments from five subjects before they were given 150 or 300 mg of aspirin and at various intervals afterward. We then measured prostacyclin (PGI 2 ) synthesis with a radioimmunoassay for its stable metabolite, 6-keto-prostaglandin F 1α . Platelet production of thromboxane A 2 was measured with a radioimmunoassay for its stable metabolite, thromboxane B 2 . Two hours after aspirin had been given, 81 to 100 per cent inhibition of PGI 2 synthesis was demonstrated; 86 per cent inhibition was still evident in one subject tested eight hours after administration. Simultaneously, platelet production of thromboxane B 2 was completely inhibited for more than 24 hours. We conclude that there is little difference between the initial inhibitory response of platelet cyclooxygenase and that of vessel-wall cyclooxygenase to these doses of aspirin. Our results also indicate that in male subjects the prolonged template bleeding time after aspirin is not the consequence of selective inhibition of platelet production of thromboxane. (N Engl J Med. 1981; 304:76–9.) IT has been recognized for several years that aspirin inhibits platelet aggregation by acetylating the enzyme cyclooxygenase. 1 , 2 However, the potentially beneficial effect of aspirin on prostaglandin biosynthesis in platelets may be offset by a similar inhibitory effect on prostacyclin (PGI 2 ) generated by normal vascular endothelial cells. In this study, we measured PGI 2 synthesized by segments of veins obtained before a single low dose of aspirin was given to normal volunteers and at various times afterward. The results were compared with the inhibitory effect of aspirin on platelet production of thromboxane A 2 (TXA 2 ), determined in . . .