Salvioni A, Marenzi G, Lauri G, Giraldi F, Perego G B, Grazi S, Guazzi M D
Istituto di Cardiologia dell'Università degli Studi, Milan, Italy.
Am Heart J. 1994 Sep;128(3):472-6. doi: 10.1016/0002-8703(94)90619-x.
In vitro and in vivo studies have shown both an inhibition and an activation of platelets after thrombolysis in acute myocardial infarction. Plasma beta-thromboglobulin, a marker of platelet activity, was evaluated daily during the first week after myocardial infarction in 24 patients who received intravenous streptokinase (group 1) and 26 who did not (group 2). On admission, levels of beta-thromboglobulin, as compared to those in healthy subjects (35 +/- 9 IU/ml), were similarly augmented in group 1 (105 +/- 27 IU/ml) and in group 2 (115 +/- 30 IU/ml); 3 hours later, values averaged 191 +/- 58 IU/ml in group 1 (p < 0.001 vs baseline) and 95 +/- 28 IU/ml in group 2 (not significant vs baseline; p < 0.001 between the two groups). From the second to the seventh day, beta-thromboglobulin augmented in those patients in both groups with postinfarction angina. From day 5 to day 7, patients of group 1 without angina had lower beta-thromboglobulin levels than patients of group 2 who had no symptoms. The lowest levels of platelet activity were observed in group 1 reperfused patients. These data indicate that in myocardial infarction an early platelet activation takes place that is enhanced by thrombolytic treatment; recurrence of angina is associated with persistent activation; in the absence of recurrent angina, thrombolysis can limit late platelet activation.
体外和体内研究均显示，急性心肌梗死溶栓治疗后血小板既有抑制又有激活现象。在24例接受静脉链激酶治疗的患者（第1组）和26例未接受静脉链激酶治疗的患者（第2组）中，在心肌梗死后第一周每天评估血浆β-血小板球蛋白（一种血小板活性标志物）。入院时，与健康受试者（35±9 IU/ml）相比，第1组（105±27 IU/ml）和第2组（115±30 IU/ml）的β-血小板球蛋白水平同样升高；3小时后，第1组的值平均为191±58 IU/ml（与基线相比，p<0.001），第2组为95±28 IU/ml（与基线相比无显著性差异；两组之间p<0.001）。从第二天到第七天，两组中发生梗死后心绞痛的患者β-血小板球蛋白水平升高。从第5天到第7天，第1组无胸痛的患者β-血小板球蛋白水平低于第2组无症状的患者。第1组再灌注患者的血小板活性水平最低。这些数据表明，在心肌梗死中，早期会发生血小板激活，溶栓治疗会增强这种激活；心绞痛复发与持续激活有关；在无心绞痛复发的情况下，溶栓可限制晚期血小板激活。
