As the pathogenesis of arterial thrombosis often includes platelet adhesion and aggregation, antiplatelet agents are commonly used to prevent thromboembolic events. Here, a new microfluidic method without additional adhesion protein modification was developed to quantify the inhibitory effect of antiplatelet drugs on the adhesion and aggregation behavior of platelets on glass surfaces under physiological flow conditions. Polydimethylsiloxane (PDMS)-glass microfluidic chips were fabricated by soft photolithography. Blood samples from healthy volunteers or patients before and after taking anti-platelet drugs flowed through the microchannels at wall shear rates of 300 s-1 and 1500 s-1, respectively. The time to reach 2.5% platelet aggregation surface coverage (Ti), surface coverage (A150s), and mean fluorescence intensity (F150s) were used as quantitative indicators. Aspirin (80 μM) prolonged Ti and reduced F150s. Alprostadil, ticagrelor, eptifibatide，and tirofiban prolonged Ti and reduced A150s and F150s in a concentration-dependent manner, while high concentrations of alprostadil did not completely inhibit platelet aggregation. Aspirin combined with ticagrelor synergistically inhibited platelet adhesion and aggregation; GPIb-IX- von Willebrand Factor (vWF) inhibitors partially inhibited platelet aggregation and the inhibition was more pronounced at 1500s-1 than at 300s-1. Patient administration of aspirin or (and) clopidogrel inhibited platelet adhesion and aggregation on the glass surface under flow conditions. This technology is capable of distinguishing the pharmacological effects of various antiplatelet drugs on inhibition of platelet adhesion aggregation on glass surface under physiological flow conditions, which providing a new way to develop microfluidic platelet function detection method without additional adhesive protein modification for determining the inhibitory effects of antiplatelet drugs in the clinical setting.

中文翻译：

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抗血小板剂在生理流动条件下抑制玻璃表面上的血小板粘附和聚集：针对无需额外粘附蛋白修饰的微流体血小板功能测定。

由于动脉血栓形成的发病机制通常包括血小板粘附和聚集，因此通常使用抗血小板药物来预防血栓栓塞事件。这里，开发了一种无需额外粘附蛋白修饰的新微流体方法，用于量化生理流动条件下抗血小板药物对玻璃表面血小板粘附和聚集行为的抑制作用。聚二甲基硅氧烷（PDMS）玻璃微流控芯片是通过软光刻技术制造的。服用抗血小板药物之前和之后的健康志愿者或患者的血液样本分别以 300 s-1 和 1500 s-1 的壁剪切速率流过微通道。以血小板聚集达到2.5%的时间(Ti)、表面覆盖度(A150s)、平均荧光强度(F150s)作为定量指标。阿司匹林 (80 μM) 延长 Ti 并降低 F150。前列地尔、替格瑞洛、依替巴肽和替罗非班以浓度依赖性方式延长Ti并降低A150和F150，而高浓度前列地尔并不能完全抑制血小板聚集。阿司匹林联合替格瑞洛协同抑制血小板粘附和聚集；GPIb-IX-冯维勒布兰德因子（vWF）抑制剂部分抑制血小板聚集，并且这种抑制在1500s-1时比在300s-1时更明显。在流动条件下，患者服用阿司匹林或（和）氯吡格雷可抑制血小板在玻璃表面的粘附和聚集。该技术能够区分多种抗血小板药物在生理流动条件下抑制玻璃表面血小板粘附聚集的药理作用，为开发无需额外粘附蛋白修饰的微流控血小板功能检测方法来测定其抑制作用提供了新途径。临床上的抗血小板药物。