Kim S W, Wisniewski S, Lee E S, Winn M L
J Biomed Mater Res. 1977 Jan;11(1):23-31. doi: 10.1002/jbm.820110104.
Thrombus formation on a foreign surface is a complicated process, involving many factors. However, there is little doubt that a foreign surface adsorbs plasma proteins upon blood contact and that the nature of this adsorbed layer may determine the mechanism of platelet adhesion and aggregation. The adhesion and aggregation of platelets play an important role in the initial events of thrombus formation on a foreign surface. In this work, adsorption studies using human blood plasma were done on several polymer surfaces. Some drugs which prevent platelet adhesion were utilized to verify the proposed mechanism for platelet adhesion which includes glycosyl transferase reaction. Also, adsorption and release of fatty acid salts, including fatty acid-bonded albumin, were investigated at different polymer interfaces. It is postulated that adsorbed fatty acid salts are released from the surface upon contact with plasma to form a high local concentration of fatty acid, and that this fatty acid suspension would cause platelet aggregation at the interface.
异物表面血栓形成是一个复杂的过程,涉及许多因素。然而,毫无疑问,异物表面在与血液接触时会吸附血浆蛋白,并且这种吸附层的性质可能决定血小板黏附和聚集的机制。血小板的黏附和聚集在异物表面血栓形成的初始事件中起重要作用。在这项工作中,使用人血浆对几种聚合物表面进行了吸附研究。利用一些防止血小板黏附的药物来验证所提出的包括糖基转移酶反应的血小板黏附机制。此外,还研究了不同聚合物界面处脂肪酸盐(包括脂肪酸结合白蛋白)的吸附和释放。据推测,吸附的脂肪酸盐在与血浆接触时从表面释放,形成高局部浓度的脂肪酸,并且这种脂肪酸悬浮液会导致界面处的血小板聚集。