Uchiyama S, Yamazaki M, Maruyama S, Handa M, Ikeda Y, Fukuyama M, Itagaki I
Department of Neurology, Tokyo Women's Medical College, Japan.
Stroke. 1994 Aug;25(8):1547-51. doi: 10.1161/01.str.25.8.1547.
Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents.
The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in citrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents.
Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shear-induced platelet aggregation with platelet count, agonist-induced platelet aggregation, fibrinogen level, or beta-thromboglobulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it.
These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the increase of larger von Willebrand factor multimers, and is corrected by ticlopidine but not by low-dose aspirin.
最近有证据表明，剪切力诱导的血小板聚集是动脉分叉处或狭窄部位血栓形成的重要机制。我们使用一种新装置测量了脑缺血患者剪切力诱导的血小板聚集情况，并研究了其与其他止血参数的相关性以及抗血小板药物的作用。
研究对象为75例脑缺血患者和26例对照者。通过基于比浊法的锥板流动腔施加高剪切应力（108达因/平方厘米），在枸橼酸化富血小板血浆中诱导血小板聚集。我们研究了检测结果与止血参数的相关性以及抗血小板药物的作用。
与对照者相比，21例动脉粥样硬化血栓形成性卒中患者和12例短暂性脑缺血发作患者的剪切力诱导血小板聚集增加，但11例心源性脑栓塞性卒中患者和31例腔隙性卒中患者未出现增加。剪切力诱导的血小板聚集与血小板计数、激动剂诱导的血小板聚集、纤维蛋白原水平或β-血小板球蛋白水平无显著相关性。剪切力诱导聚集的程度与血管性血友病因子抗原水平无关，但与较大血管性血友病因子多聚体的量显著相关。口服阿司匹林（81毫克/天）未抑制剪切力诱导的血小板聚集，而口服噻氯匹定（200毫克/天）可显著抑制。
这些结果表明，动脉粥样硬化血栓形成性卒中和短暂性脑缺血发作患者的剪切力诱导血小板聚集增加，与较大血管性血友病因子多聚体的增加相关，且可被噻氯匹定纠正，但不能被小剂量阿司匹林纠正。
