Platelet and vascular function during coronary thrombolysis with tissue-type plasminogen activator.
Platelet and vascular function during coronary thrombolysis with tissue-type plasminogen activator.
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使用组织型纤溶酶原激活剂进行冠状动脉溶栓期间的血小板和血管功能。
DOI：
10.1161/01.cir.80.6.1718
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发表时间：
1989
期刊：
影响因子：
37.8
通讯作者：
Fitzgerald,DJ
中科院分区：
文献类型：
--
作者：
Kerins,DM;Roy,L;FitzGerald,GA;Fitzgerald,DJ
血小板活化可能限制人冠状动脉溶栓过程中对组织型纤溶酶原激活剂（t-PA）的反应。作为血小板活化的指标，我们评估了急性心肌梗死患者静脉t-PA冠状动脉溶栓过程中血栓素A2的生物合成。静脉注射t-PA后，尿2，3-二去甲-血栓烷B2（血栓烷A2的代谢产物）升高至峰值3，327 +/- 511 pg/mg肌酐（n = 12），并在48小时内保持升高。口服阿司匹林325 mg（n = 6）预处理可消除这种增加，表明血栓烷A2的从头生物合成，而不是再灌注期间预先形成的代谢产物的洗脱。前列环素（PGI 2）的生物合成（通过2，3-二去甲-6-酮-PGF 1 α的排泄测定）也在t-PA给药后增加。然而，与再灌注失败的患者（118 +/- 30 ng.hr/mg肌酐，p <0.05）相比，再灌注患者（28 +/-3.3ng.hr/mg肌酐）的这种增加不太明显。这些数据提供了t-PA冠状动脉溶栓过程中血小板活化的证据。在再灌注患者中，PGI 2生物合成的减少可能是血管再灌注损伤的标志，并可能进一步放大血小板活化。
Platelet activation may limit the response to tissue-type plasminogen activator (t-PA) during coronary thrombolysis in humans. As an index of platelet activation, we assessed thromboxane A2 biosynthesis during coronary thrombolysis with intravenous t-PA in patients with acute myocardial infarction. Urinary 2,3-dinor-thromboxane B2, a metabolite of thromboxane A2, was increased to a peak of 3,327 +/- 511 pg/mg creatinine (n = 12) following administration of intravenous t-PA and remained elevated for 48 hours. This increase was abolished by pretreatment with aspirin 325 mg orally (n = 6), indicating de novo biosynthesis of thromboxane A2 rather than washout of preformed metabolites during reperfusion. Prostacyclin (PGI2) biosynthesis, determined by excretion of 2,3-dinor-6-keto-PGF1 alpha, also increased after t-PA administration. However, this increase was less pronounced in patients who reperfused (28 +/- 3.3 ng.hr/mg creatinine) than in patients who failed to reperfuse (118 +/- 30 ng.hr/mg creatinine, p less than 0.05). These data provide evidence of platelet activation during coronary thrombolysis with t-PA. In patients who reperfuse, the reduction in PGI2 biosynthesis may be a marker of reperfusion injury to the vasculature and may further amplify platelet activation.