尿激酶溶栓治疗对急性脑梗死患者活化血小板GPIIb/IIIa表达的作用
北京大学第一医院神经内科 (100034)
【摘要】目的：探讨急性脑梗死患者尿激酶溶栓治疗后血小板活化状态的变化。方法：应用流式细胞仪(FCM)三色荧光抗体的方法测定活化血小板的GPIIb-IIIa阳性细胞百分率和平均荧光强度。急性脑梗死患者在发病6 h以内采用尿激酶溶栓治疗，尿激酶剂量150万U，静脉点滴30 min，共15例。溶栓治疗组分别在溶栓前、溶栓后1 h、6 h、1 d采血，结果与常规治疗组和健康对照组进行比较。结果：急性脑梗死患者活化血小板的GPIIb/IIIa阳性细胞百分率和平均荧光强度显著高于健康对照组；但急性脑梗死患者常规治疗前后无显著性变化。大多数急性脑梗死患者尿激酶静脉溶栓治疗后GPIIb/IIIa阳性细胞百分率和平均荧光强度轻度下降, 尿激酶治疗导致的活化血小板降低在治疗后6 h达统计学显著性意义，但溶栓治疗后1 h和1 d无显著性变化。少数急性脑梗死患者尿激酶静脉溶栓治疗后GPIIb/IIIa阳性细胞百分率和平均荧光强度增高，尤其是表现再梗死综合症的3例患者增高非常显著。结论：尿激酶既可激活血小板，也可降低血小板的功能。为了防止尿激酶溶栓后的血管再闭塞或脑出血，应严密观察溶栓后血小板的功能，并因人而异加用抗血小板药物治疗。
, 百拇医药
Effect of Urokinase on-expression of platelet glycoprotein IIb/IIIa in patients with acute brain infarction
HE Mao-lin, CAO Lin, ZHAO Hai-yan, et al.
Department of Neurology, First Affiliated Hospital, Peking University, Beijing 100034
【Abstract】Objective: To assess platelet activation after urokinase thrombolysis in patients with acute brain infarction. Methods: Expression of platelet glycoprotein IIb/IIIa (GP IIb/IIIa) were serially evaluated on admission and 1 hour, 6 hours, 24 hours after intravenous thrombolysis with 1.5 million units of UK over 30 min in 15 patients with acute brain infarction which treated within 6 hours of symptom onset by whole blood flow cytometry, and compared to the measurements in the healthy control subjects and the routine-treatment subjects. Results: The patients with acute brain infarction showed highly significant increases in the percentage of GPIIb/IIIa-positive circulating platelets and the mean fluorescene intensity at the baseline and the follow-up levels, compared with the healthy subjects .But there was no differences between pre-treatment and post treatment in routine-treatment subjects. Platelet activation were inhibited slightly after thrombolytic therapy in most of the cases. The attenuated platelet activation reached significance 6 hours after thrombolysis compared with the baselines. But no significant differences could be detected between the baselines and the assessments 1 hour or 24 hours after thrombolysis. Platelet activation were enhanced after thrombolytic therapy in some cases, especially 3 patients with reinfarction syndrome. Conclusions: Platelets can be activated or inhibited during UK thrombolysis process. Individual assessment of antiplatelet treatment during thrombolysis is desirable to prevent infarct-related artery reocclusion or intracranial hemorrhage.
【Key words】 Platelet Glycoprotein IIb/IIIa Urokinase Thrombolytic therapy, 百拇医药(贺茂林 曹凌 赵海燕等)
【摘要】目的：探讨急性脑梗死患者尿激酶溶栓治疗后血小板活化状态的变化。方法：应用流式细胞仪(FCM)三色荧光抗体的方法测定活化血小板的GPIIb-IIIa阳性细胞百分率和平均荧光强度。急性脑梗死患者在发病6 h以内采用尿激酶溶栓治疗，尿激酶剂量150万U，静脉点滴30 min，共15例。溶栓治疗组分别在溶栓前、溶栓后1 h、6 h、1 d采血，结果与常规治疗组和健康对照组进行比较。结果：急性脑梗死患者活化血小板的GPIIb/IIIa阳性细胞百分率和平均荧光强度显著高于健康对照组；但急性脑梗死患者常规治疗前后无显著性变化。大多数急性脑梗死患者尿激酶静脉溶栓治疗后GPIIb/IIIa阳性细胞百分率和平均荧光强度轻度下降, 尿激酶治疗导致的活化血小板降低在治疗后6 h达统计学显著性意义，但溶栓治疗后1 h和1 d无显著性变化。少数急性脑梗死患者尿激酶静脉溶栓治疗后GPIIb/IIIa阳性细胞百分率和平均荧光强度增高，尤其是表现再梗死综合症的3例患者增高非常显著。结论：尿激酶既可激活血小板，也可降低血小板的功能。为了防止尿激酶溶栓后的血管再闭塞或脑出血，应严密观察溶栓后血小板的功能，并因人而异加用抗血小板药物治疗。
, 百拇医药
Effect of Urokinase on-expression of platelet glycoprotein IIb/IIIa in patients with acute brain infarction
HE Mao-lin, CAO Lin, ZHAO Hai-yan, et al.
Department of Neurology, First Affiliated Hospital, Peking University, Beijing 100034
【Abstract】Objective: To assess platelet activation after urokinase thrombolysis in patients with acute brain infarction. Methods: Expression of platelet glycoprotein IIb/IIIa (GP IIb/IIIa) were serially evaluated on admission and 1 hour, 6 hours, 24 hours after intravenous thrombolysis with 1.5 million units of UK over 30 min in 15 patients with acute brain infarction which treated within 6 hours of symptom onset by whole blood flow cytometry, and compared to the measurements in the healthy control subjects and the routine-treatment subjects. Results: The patients with acute brain infarction showed highly significant increases in the percentage of GPIIb/IIIa-positive circulating platelets and the mean fluorescene intensity at the baseline and the follow-up levels, compared with the healthy subjects .But there was no differences between pre-treatment and post treatment in routine-treatment subjects. Platelet activation were inhibited slightly after thrombolytic therapy in most of the cases. The attenuated platelet activation reached significance 6 hours after thrombolysis compared with the baselines. But no significant differences could be detected between the baselines and the assessments 1 hour or 24 hours after thrombolysis. Platelet activation were enhanced after thrombolytic therapy in some cases, especially 3 patients with reinfarction syndrome. Conclusions: Platelets can be activated or inhibited during UK thrombolysis process. Individual assessment of antiplatelet treatment during thrombolysis is desirable to prevent infarct-related artery reocclusion or intracranial hemorrhage.
【Key words】 Platelet Glycoprotein IIb/IIIa Urokinase Thrombolytic therapy, 百拇医药(贺茂林 曹凌 赵海燕等)