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首页> 外文期刊>Artificial Organs >Paradoxical Effect of Nonphysiological Shear Stress on Platelets and von Willebrand Factor
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Paradoxical Effect of Nonphysiological Shear Stress on Platelets and von Willebrand Factor

机译：非生理性剪应力对血小板和von Willebrand因子的悖论效应

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Blood can become hypercoagulable by shear-induced platelet activation and generation of microparticles. It has been reported that nonphysiological shear stress (NPSS) could induce shedding of platelet receptor glycoprotein (GP) Ib, which may result in an opposite effect to hemostasis. The aim of this study was to investigate the influence of the NPSS on platelets and von Willebrand factor (vWF). Human blood was exposed to two levels of NPSS (25Pa, 125Pa) with an exposure time of 0.5s, generated by using a novel blood-shearing device. Platelet activation (P-selectin expression, GPIIb/IIIa activation and generation of microparticles) and shedding of three platelet receptors (GPIb, GPVI, GPIIb/IIIa) in sheared blood were quantified using flow cytometry. Aggregation capacity of sheared blood induced by ristocetin and collagen was evaluated using an aggregometer. Shear-induced vWF damage was characterized with Western blotting. Consistent with the published data, the NPSS caused significantly more platelets to become activated with increasing NPSS level. Meanwhile, the NPSS induced the shedding of platelet receptors. The loss of the platelet receptors increased with increasing NPSS level. The aggregation capacity of sheared blood induced by ristocetin and collagen decreased. There was a loss of high molecular weight multimers (HMWMs) of vWF in sheared blood. These results suggest that the NPSS induced a paradoxical effect. More activated platelets increase the risk of thrombosis, while the reduction in platelet receptors and the loss of HMWM-vWF increased the propensity of bleeding. The finding might provide a new perspective to understand thrombosis and acquired bleeding disorder in patients supported with blood contacting medical devices.
机译：血液可以通过剪切诱导的血小板活化和微粒的产生而变得高度凝集。据报道，非生理切应力（NPSS）可能诱导血小板受体糖蛋白（GP）Ib脱落，这可能导致与止血相反的作用。这项研究的目的是调查NPSS对血小板和von Willebrand因子（vWF）的影响。使用新型血液剪切装置将人血暴露于两种水平的NPSS（25Pa，125Pa）中，暴露时间为0.5s。使用流式细胞仪对剪切血中的血小板活化（P-选择蛋白表达，GPIIb / IIIa活化和微粒生成）和三种血小板受体（GPIb，GPVI，GPIIb / IIIa）的脱落进行定量。使用凝集计评估由瑞斯托菌素和胶原蛋白诱导的剪切血的聚集能力。剪切诱导的vWF损伤用蛋白质印迹法表征。与已公布的数据一致，NPSS导致随着NPSS水平的提高，更多的血小板被激活。同时，NPSS引起血小板受体的脱落。血小板受体的丢失随着NPSS水平的增加而增加。瑞斯托霉素和胶原蛋白诱导的剪切血的聚集能力降低。剪切血中vWF的高分子量多聚体（HMWM）丢失。这些结果表明，NPSS引起自相矛盾的作用。活化的血小板更多会增加血栓形成的风险，而血小板受体的减少和HMWM-vWF的损失会增加出血的倾向。这一发现可能为了解血液接触医疗器械患者的血栓形成和获得性出血性疾病提供了新的视角。

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