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小剂量阿司匹林后前列环素和血小板血栓素A2的抑制作用。

Inhibition of prostacyclin and platelet thromboxane A2 after low-dose aspirin.

作者信息

Preston F E, Whipps S, Jackson C A, French A J, Wyld P J, Stoddard C J

出版信息

N Engl J Med. 1981 Jan 8;304(2):76-9. doi: 10.1056/NEJM198101083040203.

Abstract

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 (PGI2) synthesis with a radioimmunoassay for its stable metabolite, 6-keto-prostaglandin F1 alpha. Platelet production of thromboxane A2 was measured with a radioimmunoassay for its stable metabolite, thromboxane B2. Two hours after aspirin had been given, 81 to 100 per cent inhibition of PGI2 synthesis was demonstrated; 86 per cent inhibition was still evident in one subject tested eight hours after administration. Simultaneously, platelet production of thromboxane B2 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.

摘要

为比较阿司匹林对血管壁和血小板合成前列腺素的抑制作用,我们在五名受试者服用150或300毫克阿司匹林之前及其后不同时间段采集了静脉段。然后,我们用放射免疫分析法测定前列环素(PGI2)的稳定代谢产物6-酮-前列腺素F1α,以检测前列环素的合成。用放射免疫分析法测定血栓素A2的稳定代谢产物血栓素B2,以检测血小板生成血栓素A2的情况。服用阿司匹林两小时后,PGI2合成受到81%至100%的抑制;在给药八小时后检测的一名受试者中,86%的抑制作用仍然明显。同时,血栓素B2的血小板生成被完全抑制超过24小时。我们得出结论,血小板环氧化酶和血管壁环氧化酶对这些剂量阿司匹林的初始抑制反应几乎没有差异。我们的结果还表明,在男性受试者中,阿司匹林后延长的模板出血时间并非选择性抑制血小板生成血栓素的结果。

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