O'Brien J R, Salmon G P
Central Laboratory, St. Mary's Hospital, Portsmouth, Hants., UK.
Adv Exp Med Biol. 1990;281:287-96. doi: 10.1007/978-1-4615-3806-6_30.
We have published (1) evidence indicating that high shearing forces alone applied to platelets expose and activate a unique domain on glycoprotein IIb/IIIa (GPIIb/IIIa) at the platelet surface. In the presence of von Willebrand's factor (vWf) and divalent cations the platelets will aggregate. This paper reviews the extensive literature on high shear effects. It describes a device in which high shear produced by forcing heparinised whole blood through a complex filter normally results in platelet activation; the platelets aggregate and then block the filter. This system is inhibited by antibodies to GPIIb/IIIa and to vWf: fibrinogen is apparently not involved. The same antibodies to GPIIb/IIIa and vWf prevent high shear induced thrombosis occurring in vivo in animal models. The filter blockage is not influenced by aspirin, heparin and ticlopidine and so involves a different mechanism from the aspirin sensitive mechanisms involved in clinical thrombosis prevention in vivo in man. While there are a number of unexplained phenomena in this global test nevertheless this filter model is a simple way of studying a recently recognised pathway which is almost certainly involved in thrombogenesis in man.
我们已经发表了（1）相关证据，表明仅对血小板施加高剪切力会使血小板表面糖蛋白IIb/IIIa（GPIIb/IIIa）上的一个独特结构域暴露并激活。在存在血管性血友病因子（vWf）和二价阳离子的情况下，血小板会发生聚集。本文综述了关于高剪切力影响的大量文献。它描述了一种装置，通过迫使肝素化全血通过一个复杂的过滤器产生高剪切力，通常会导致血小板激活；血小板聚集然后堵塞过滤器。该系统受到针对GPIIb/IIIa和vWf的抗体的抑制：纤维蛋白原显然未参与其中。针对GPIIb/IIIa和vWf的相同抗体可防止动物模型体内发生高剪切力诱导的血栓形成。过滤器堵塞不受阿司匹林、肝素和噻氯匹定的影响，因此涉及一种与人体临床血栓形成预防中涉及的阿司匹林敏感机制不同的机制。虽然在这个整体测试中有许多无法解释的现象，但这个过滤器模型是研究一种最近才被认识到的途径的简单方法，而这种途径几乎肯定与人类血栓形成有关。
