The regions with high non-physiological shear stresses (NPSS) are inevitable in blood-contacting medical devices (BCMDs) used for mechanically assisted circulatory support. NPSS can cause platelet activation and receptor shedding potentially resulting in the alteration of hemostatic function. In this study, we developed a dissipative particle dynamics model to characterize clot formation (platelet–collagen and inter-platelet adhesion) of NPSS-traumatized blood at a vascular injury site. A rectangular tube of 50 × 50 × 200 µm with an 8 × 8 µm collagen-coated area was modeled as a small blood vessel and perfusion with blood. Clot formation dynamics during perfusion was simulated. NPSS-traumatized blood was modeled to have more activated platelet and fewer adhesion receptors with weakened inter-platelet binding. Computational results showed that clots grew at a faster rate while the structure of the clots was less stable and collapsed more frequently for NPSS-traumatized blood compared with normal blood. The finding that NPSS-traumatized platelets could result in quicker but more easily breakable blood clots at injury sites may explain why increased risks of thrombotic and bleeding complications occurred concurrently in patients implanted with BCMDs.

中文翻译：

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用耗散粒子动力学方法模拟流动中剪切损伤血小板的凝块形成

在用于机械辅助循环支持的血液接触医疗设备 (BCMD) 中，具有高非生理剪切应力 (NPSS) 的区域是不可避免的。NPSS 可引起血小板活化和受体脱落，从而可能导致止血功能的改变。在这项研究中，我们开发了一种耗散粒子动力学模型来表征血管损伤部位 NPSS 创伤血液的凝块形成（血小板-胶原蛋白和血小板间粘附）。一个 50 × 50 × 200 µm 的矩形管和一个 8 × 8 µm 的胶原涂层区域被建模为一个小血管和血液灌注。模拟了灌注过程中的凝块形成动力学。NPSS 创伤血液被建模为具有更多活化的血小板和更少的粘附受体，并且血小板间结合减弱。计算结果表明，与正常血液相比，NPSS 创伤血液的凝块生长速度更快，而凝块的结构不太稳定，塌陷更频繁。NPSS 创伤性血小板可能导致损伤部位更快但更容易破裂的血凝块的发现可以解释为什么植入 BCMD 的患者同时发生血栓和出血并发症的风险增加。