Blood flow disorders are often the result of the non-physiological narrowing of blood arteries caused by atherosclerosis and thrombus. The blood then proceeds through rising-peak-decreasing phases as it passes through the narrow area. Although abnormally high shear is known to activate platelets, the shear process that platelets undergo in small arteries is complex. Thus, understanding how each shear phase affects platelet activation can be used to improve antiplatelet therapy and decrease the risk of side effects like bleeding. Blood samples were sheared (68.8 ms,5200 s⁻¹) in vitro by the microfluidic technique, and platelet activation levels (P-selectin and integrin αIIbβ3) and von Willebrand factor (vWF) binding to platelets were analyzed by flow cytometry. Post-stenosis platelet aggregation was dynamically detected using microfluidic technology. We studied TXA2, P2Y₁₂-ADP, and integrin αIIbβ3-fibrinogen receptor pathways by adding antiplatelet drugs, such as acetylsalicylic acid (ASA, an active ingredient of aspirin that inhibits platelet metabolism), ticagrelor (hinders platelet activation), and tirofiban (blocks integrin αIIbβ3 receptor) in vitro, respectively, to determine platelet activation function mediated by transient non-physiological high shear rates. We demonstrated that platelets can be activated under transient pathological high shear rates. The shear rise and fall phases influenced shear-induced platelet activation by regulating the binding of vWF to platelets. The degree of platelet activation and aggregation increased with multiple shear rise and fall phases. ASA did not inhibit shear-mediated platelet activation, but ticagrelor and tirofiban effectively inhibited shear-mediated platelet activation. Our data demonstrated that the shear rise and fall phases play an important role in shear-mediated platelet activation and promote platelet activation and aggregation in a vWF-dependent manner. Blocking integrin αIIbβ3 receptor and hindering P2Y₁₂-ADP were beneficial to reducing shear-mediated platelet activation.

血流障碍往往是动脉粥样硬化和血栓引起的血动脉非生理性狭窄的结果。然后，血液在通过狭窄区域时会经历上升-峰值-下降阶段。尽管已知异常高的剪切力会激活血小板，但血小板在小动脉中经历的剪切过程很复杂。因此，了解每个剪切相如何影响血小板活化可用于改善抗血小板治疗并降低出血等副作用的风险。通过微流控技术在体外剪切血样（68.8 ms，5200 s ^-1），并通过流式细胞术分析血小板活化水平（P-选择素和整合素αIIbβ3）和与血小板结合的冯维勒布兰德因子（vWF）。使用微流体技术动态检测狭窄后血小板聚集。我们通过添加抗血小板药物，例如乙酰水杨酸（ASA，阿司匹林的一种活性成分，抑制血小板代谢）、替格瑞洛（阻碍血小板活化）和替罗非班（_阻断整合素αIIbβ3受体）分别在体外测定瞬时非生理性高剪切速率介导的血小板活化功能。我们证明血小板可以在短暂的病理性高剪切速率下被激活。剪切力上升和下降阶段通过调节 vWF 与血小板的结合来影响剪切诱导的血小板活化。血小板活化和聚集的程度随着多个剪切上升和下降阶段而增加。 ASA 不抑制剪切介导的血小板活化，但替格瑞洛和替罗非班有效抑制剪切介导的血小板活化。我们的数据表明，剪​​切上升和下降阶段在剪切介导的血小板活化中发挥重要作用，并以 vWF 依赖性方式促进血小板活化和聚集。阻断整合素αIIbβ3受体和阻碍P2Y ₁₂ -ADP有利于减少剪切介导的血小板活化。