Fogelson Aaron L, Guy Robert D
Department of Mathematics, University of Utah, Salt Lake City, Utah 84112, USA.
Math Med Biol. 2004 Dec;21(4):293-334. doi: 10.1093/imammb21.4.293.
A model is developed to describe the formation of platelet thrombi in coronary-artery-sized blood vessels. It involves interactions among a viscous, incompressible fluid; populations of non-activated and activated platelets; activating chemicals; and the vessel walls. Adhesion of platelets to the injured wall and cohesion between activated platelets is modelled using distributions of elastic links which generate stresses that can influence the fluid motion. The first version of the model presented involves two spatial scales: the microscale of the platelets and the macroscale of the vessel. A closure approximation is introduced that allows essential microscale behaviour to be computed while eliminating the necessity to explicitly track events on this scale. Computational methods are presented that meet the diverse challenges posed by the coupled nonlinear partial differential equations of the model and by the complex geometry of the constricted vessels in which the thrombosis simulations are carried out. Simulation results demonstrate that the model can produce thrombi that grow to occlude the vessel, that shear-stress exerted by the fluid on the thrombi can modify their subsequent growth and cause remodelling of their shape through small-scale local changes or large-scale structural breakup.
开发了一个模型来描述冠状动脉大小血管中血小板血栓的形成。它涉及粘性、不可压缩流体、未激活和激活的血小板群体、激活化学物质以及血管壁之间的相互作用。使用弹性连接分布对血小板与受损壁的粘附以及激活血小板之间的内聚进行建模,弹性连接分布会产生可影响流体运动的应力。所呈现的模型的第一个版本涉及两个空间尺度:血小板的微观尺度和血管的宏观尺度。引入了一种封闭近似,使得能够计算基本的微观尺度行为,同时消除了在此尺度上明确跟踪事件的必要性。提出了计算方法,以应对由模型的耦合非线性偏微分方程以及进行血栓形成模拟的狭窄血管的复杂几何形状所带来的各种挑战。模拟结果表明,该模型能够产生生长到阻塞血管的血栓,流体对血栓施加的剪切应力可以改变其后续生长,并通过小规模局部变化或大规模结构破裂导致其形状重塑。