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Modelling thrombosis using dissipative particle dynamics method

机译:使用耗散粒子动力学方法对血栓形成进行建模

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摘要

Aim. Arterial occlusion is a leading cause of cardiovascular disease. The main mechanism causing vessel occlusion is thrombus formation, which may be initiated by the activation of platelets. The focus of this study is on the mechanical aspects of platelet-mediated thrombosis which includes the motion, collision, adhesion and aggregation of activated platelets in the blood. A review of the existing continuum-based models is given. A mechanical model of platelet accumulation onto the vessel wall is developed using the dissipative particle dynamics (DPD) method in which the blood (i.e. colloidal-composed medium) is treated as a group of mesoscale particles interacting through conservative, dissipative, attractive and random forces.Methods. Colloidal fluid components (plasma and platelets) are discretized by mesoscopic (micrometre-size) particles that move according to Newton's law. The size of each mesoscopic particle is small enough to allow tracking of each constituent of the colloidal fluid, but significantly larger than the size of atoms such that, in contrast to the molecular dynamics approach, detailed atomic level analysis is not required.Results. To test this model, we simulated the deposition of platelets onto the wall of an expanded tube and compared our computed results with the experimental data of Karino et al. (Miscrovasc. Res. >17, 238–269, 1977). By matching our simulations to the experimental results, the platelet aggregation/adhesion binding force (characterized by an effective spring constant) was determined and found to be within a physiologically reasonable range.Conclusion. Our results suggest that the DPD method offers a promising new approach to the modelling of platelet-mediated thrombosis. The DPD model includes interaction forces between platelets both when they are in the resting state (non-activated) and when they are activated, and therefore it can be extended to the analysis of kinetics of binding and other phenomena relevant to thrombosis.
机译:目标。动脉闭塞是心血管疾病的主要原因。引起血管闭塞的主要机制是血栓形成,这可能是由血小板活化引起的。这项研究的重点是血小板介导的血栓形成的机械方面,包括血液中活化的血小板的运动,碰撞,粘附和聚集。审查了现有的基于连续体的模型。使用耗散粒子动力学(DPD)方法建立了血小板在血管壁上积聚的力学模型,该方法将血液(即胶体组成的介质)视为通过保守,耗散,吸引力和随机力相互作用的一组中尺度粒子。方法。胶体流体成分(血浆和血小板)由根据牛顿定律运动的介观(微米级)颗粒离散化。每个介观粒子的尺寸都足够小,可以跟踪胶体液的每种成分,但是比原子的尺寸大得多,因此与分子动力学方法相比,不需要详细的原子能级分析。为了测试该模型,我们模拟了血小板在扩张管壁上的沉积,并将我们的计算结果与Karino等人的实验数据进行了比较。 (Miscrovasc。Res。> 17 ,238–269,1977)。通过将我们的模拟结果与实验结果进行比较,确定了血小板聚集/粘附结合力(以有效弹簧常数为特征),并发现其在生理上合理的范围内。我们的结果表明,DPD方法为血小板介导的血栓形成提供了一种有希望的新方法。 DPD模型包括血小板在静止状态(未激活)和激活时的相互作用力,因此可以扩展到结合动力学和其他与血栓形成相关的现象的分析。

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