Thromboxane A2 in vasotonic angina pectoris: evidence from direct measurements and inhibitor trials.
Thromboxane A2 in vasotonic angina pectoris: evidence from direct measurements and inhibitor trials.
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血管紧张性心绞痛中的血栓素 A2:来自直接测量和抑制剂试验的证据。
DOI:
10.1056/nejm198104233041703
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发表时间:
1981
期刊:
影响因子:
--
通讯作者:
Oates,JA
中科院分区:
文献类型:
--
作者:
Robertson,RM;Robertson,D;Roberts,LJ;Maas,RL;FitzGerald,GA;Friesinger,GC;Oates,JA
Thromboxane A2(TxA2), an arachidonic acid metabolite causing vasoconstriction and platelet aggregation, is a putative mediator of coronary-artery vasospasm. To determine whether platelet-released TxA2causes coronary arterial vasospasm, we measured plasma thromboxane B2(TxB2, the inactive hydration product of TxA2) in the radial-artery and coronary-sinus blood of seven patients and performed therapeutic trials of antiplatelet agents in nine. Although coronary-sinus TxB2levels rose from the base line approximately fivefold with spontaneous ischemia, samples drawn early in ischemia showed no rise over base-line values. Although a 150-mg dose of aspirin reduced urinary dinor-TxB2levels by over 75 per cent, it had no effect on the course of the chronic recurrent form of angina pectoris due to vasospasm ("vasotonic angina"). Similarly, indomethacin had no effect on the frequency or duration of ischemia. TxA2is unlikely to cause vasotonic angina, but it may be released during coronary vasospasm. (N Engl J Med. 1981; 304:998–1003.)