School of Medicine, Tohoku University, 6-6-01 Aoba, Aramaki, Aoba-ku, Sendai 980-8579, Japan.
Microvasc Res. 2013 Sep;89:95-106. doi: 10.1016/j.mvr.2013.05.006. Epub 2013 Jun 4.
Thrombogenesis results from the interaction between glycoprotein receptors and their ligands, although a thrombus is affected by multiple factors such as blood flow, platelet interactions, and changes in ligand characteristics. In this study, we propose a platelet adhesion and aggregation model, focusing on the interaction between the glycoprotein receptor and its ligand. First, we conducted thrombogenesis simulations to compare physiological and pathological conditions. The results suggested that simulations of thrombogenesis differed in distribution, volume, and stability of the thrombus based on disorders of platelet adhesion, aggregation, and the activation. For example, distribution and volume were affected by the activation of GPIIb/IIIa with a GPIb/IX/V deficiency. The thrombus was also unstable, but formed from the upstream side of the injured site, with a GPIIb/IIIa deficiency. Second, we investigated thrombogenesis enhanced by the shear-induced platelet aggregation (SIPA) mechanism. The results demonstrated that the degree of SIPA decreased gradually with thrombus growth in a straight vessel. This result suggests that SIPA is a key hemostasis mechanism in an injured healthy arteriole, although it can lead to the formation of an occlusive thrombus in stenosed vessels.
血栓形成是糖蛋白受体与其配体相互作用的结果，尽管血栓受到多种因素的影响，如血流、血小板相互作用以及配体特性的变化。在本研究中，我们提出了一个血小板黏附和聚集模型，重点关注糖蛋白受体与其配体的相互作用。首先，我们进行了血栓形成模拟，以比较生理和病理条件。结果表明，基于血小板黏附和聚集以及激活的障碍，血栓形成的模拟在血栓的分布、体积和稳定性方面存在差异。例如，GPIIb/IIIa 的激活以及 GPIb/IX/V 的缺乏会影响分布和体积，而 GPIIb/IIIa 的缺乏会导致血栓不稳定，但会从损伤部位的上游形成。其次，我们研究了剪切诱导的血小板聚集（SIPA）机制增强的血栓形成。结果表明，在直血管中，随着血栓的生长，SIPA 的程度逐渐降低。这一结果表明，尽管 SIPA 在狭窄血管中可能导致闭塞性血栓形成，但它是健康损伤小动脉止血的关键机制。
