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首页> 外文期刊>Artificial Organs >Device‐induced platelet dysfunction in mechanically assisted circulation increases the risks of thrombosis and bleeding
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Device‐induced platelet dysfunction in mechanically assisted circulation increases the risks of thrombosis and bleeding

机译：机械辅助循环中的器件诱导的血小板功能障碍增加了血栓形成和出血的风险

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Abstract Thrombotic and bleeding complications are the major obstacles for expanding mechanical circulatory support (MCS) beyond the current use. While providing the needed hemodynamic support, those devices can induce damage to blood, particularly to platelets. In this study, we investigated device‐induced alteration of three major platelet surface receptors, von Willebrand factor (VWF) and associated hemostatic functions relevant to thrombosis and bleeding. Fresh human whole blood was circulated in an extracorporeal circuit with a clinical rotary blood pump (CentriMag, Abbott, Chicago, IL, USA) under the clinically relevant operating condition for 4?hours. Blood samples were examined every hour for glycoprotein (GP) IIb/IIIa activation and receptor loss of GPVI and GPIbα on the platelet surface with flow cytometry. Soluble P‐selectin in hourly collected blood samples was measured by enzyme linked immunosorbent assay to characterize platelet activation. Adhesion of device‐injured platelets to fibrinogen, collagen, and VWF was quantified with fluorescent microscopy. Device‐induced damage to VWF was characterized with western blotting. The CentriMag blood pump induced progressive platelet activation with blood circulating time. Particularly, GPIIb/IIIa activation increased from 1.1% (Base) to 11% (4?hours) and soluble P‐selectin concentration increased from 14.1?ng/mL (Base) to 26.5?ng/mL (4?hours). Those device‐activated platelets exhibited increased adhesion capacity to fibrinogen. Concurrently, the CentriMag blood pump caused progressive platelet receptor loss (GPVI and GPIbα) with blood circulating time. Specifically, MFI of the GPVI and GPIbα receptors decreased by 17.2% and 16.1% for the 4‐hours sample compared to the baseline samples, respectively. The device‐injured platelets exhibited reduced adhesion capacities to collagen and VWF. The high molecular weight multimers (HMWM) of VWF in the blood disappeared within the first hour of the circulation. Thereafter the multimeric patterns of VWF were stable. The change in the VWF multimeric pattern was different from the progressive structural and functional changes of platelets with the circulation time. This study suggested that the CentriMag blood pump could induce two opposite effects on platelets and associated hemostatic functions under a clinically relevant operating condition. The device‐altered hemostatic function may contribute to thrombosis and bleeding simultaneously as occurring in patients supported by a rotary blood pump. Device‐induced damage of platelets may be an important cause for bleeding in patients supported with rotary blood pump MCS systems relative to device‐induced loss of HMWM‐VWF.
机译：摘要血栓形成和出血并发症是扩展机械循环支持（MCS）超出当前使用的主要障碍。在提供所需的血液动力学支持的同时，这些装置可以造成对血液的损伤，特别是血小板。在这项研究中，我们研究了与血栓形成和出血相关的三个主要血小板表面受体，von Willebrand系数受体，von Willebrand因子（VWF）和相关的止血功能的改变。新鲜的人类全血在临床相关的操作条件下用临床旋转血泵（Centrimag，Abbott，芝加哥，IL，USA）在临床旋转血泵（Centrimag，Abbott，芝加哥，USA）中循环。检查血液样品每小时进行糖蛋白（GP）IIB / IIIA活化和受体损失的GPVI和GPIBα的受体损失，流式细胞术在血小板表面上。通过酶连接的免疫吸附测定测量每小时收集的血液样品中的可溶性p-选择素，以表征血小板活化。用荧光显微镜量化器件受损血小板对纤维蛋白原，胶原和VWF的粘附性。对VWF的损伤具有蛋白质印迹。 Centrimag血液泵引起血液循环时间的渐进血小板激活。特别地，GPIIB / IIIA活化从1.1％（碱）增加到11％（4？小时），可溶性p-选择素浓度从14.1〜Ng / ml（碱）增加到26.5〜Ng / ml（4？小时）。这些装置活化的血小板表现出增加纤维蛋白原的粘附能力。同时，Centrimag血液泵导致血液循环时间的进步血小板受体损失（GPVI和GPIBα）。具体地，与基线样品相比，4小时样品的GPVI和GPIBα受体的MFI分别降低了17.2％和16.1％。器件受伤的血小板对胶原蛋白和VWF的粘附能力降低。血液中VWF的高分子量多米（HMWM）在循环的第一小时内消失。此后，VWF的多聚体图案稳定。 VWF多端模式的变化与循环时间的血小板的逐渐结构和功能变化不同。该研究表明，在临床相关的运行条件下，Centrimag血液泵可以在血小板和相关止血功能上引起两个相反的影响。器件改变的止血功能可与旋转血液泵支撑的患者同时产生血栓形成和出血。装置诱导的血小板损伤可能是旋转血液泵MCS系统的患者出血的重要原因，相对于装置诱导的HMWM-VWF丧失。

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