Shear-Induced Platelet Aggregation in Normal Subjects and Stroke Patients
Shear-Induced Platelet Aggregation in Normal Subjects and Stroke Patients
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DOI：
10.1055/s-0038-1649935
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发表时间：
1995-11
影响因子：
6.7
通讯作者：
K. Konstantopoulos;J. Grotta;C. Sills;K. Wu;J. David Heliums
中科院分区：
文献类型：
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作者：
K. Konstantopoulos;J. Grotta;C. Sills;K. Wu;J. David Heliums
摘要 狭窄动脉中发生的剪切应力水平升高可能会诱导血小板聚集并引发血栓形成。使用粘度流式细胞术技术在缺血性中风患者和正常受试者组中研究了剪切诱导的血小板聚集（SIPA）。本研究纳入了 23 名非心源性缺血性中风患者，这些患者被分类为动脉粥样硬化性中风 (n = 15) 或腔隙性中风 (n = 8) 患者。结果表明，因动脉粥样硬化或血管痉挛而部分闭塞的动脉中发生的剪切应力会强烈激活和聚集血小板，这种反应在已记录脑血管动脉粥样硬化疾病的非腔隙性中风患者中更为明显。 SIPA 不受中风发作后抽血时间的影响，这表明这些血小板异常不是暂时的而是慢性的。此外，在中风发作至少一个月后研究的动脉粥样硬化性中风患者中，抗P-选择素单克隆抗体检测到的血小板活化程度和体内循环的中性粒细胞-血小板聚集体的比例显着较高。结果表明，在动脉粥样硬化性中风患者中观察到的血小板反应增强并不是缺血的结果，因此血小板活化和SIPA升高可能被认为是中风的重要危险因素。这项工作中开发的方法可能有助于表征血小板反应性，并可能有助于我们了解血栓形成机制。
Summary Elevated levels of shear stress that occur in stenotic arteries may induce platelet aggregation and initiate thrombosis. Shear-induced platelet aggregation (SIPA) was studied in groups of ischemic stroke patients and normal subjects using a viscometric-flow cytometric technique. Twenty-three patients who sustained an ischemic stroke that was not of cardiac origin were included in this study, and were classified either as atherosclerotic (n = 15) or as lacunar (n = 8) stroke patients. The results show that shear stresses at the levels which occur in arteries partially occluded by atherosclerosis or vascular spasm strongly activate and aggregate platelets, and this response is much more pronounced in non-lacunar stroke patients who had documented atherosclerotic disease of their cerebral vessels. SIPA is not affected by the time of blood drawing after the onset of stroke suggesting that these platelet abnormalities are not transient but chronic. Furthermore, the extent of platelet activation detected by an anti-P-selectin monoclonal antibody and the proportion of neutrophil-platelet aggregates circulating in vivo are significantly higher in the atherosclerotic stroke patients studied at least one month after the onset of stroke. The results indicate that the enhanced platelet responses observed in atherosclerotic stroke patients are not consequences of ischemia, and therefore both platelet activation and elevated SIPA may be considered as important risk factors for stroke. The methodology developed in this work may be useful for characterization of platelet reactivity, and may contribute to our understanding of thrombotic mechanisms.