Stangeby D Kim, Ethier C Ross
Department of Mechanical and Industrial Engineering, University of Toronto, 5 King's College Road, Toronto, Ont. M5S 3G8, Canada.
Comput Methods Biomech Biomed Engin. 2002 Jun;5(3):233-41. doi: 10.1080/10255840290010733.
Hypertension, a risk factor for atherosclerosis, increases the uptake of low density lipoproteins (LDL) by the arterial wall. Our objective in this work was to use computational modeling to identify physical factors that could be partially responsible for this effect. Fluid flow and mass transfer patterns in the lumen and wall of an arterial model were computed in a coupled manner, replicating as closely as possible previous experimental studies in which LDL uptake into the artery wall was measured in straight, excised arterial segments. Under conditions of both flow and no-flow, simulations predicted an increase in concentration polarization of LDL at the artery wall when arterial pressure was increased from 120 to 160 mmHg. However, this led to only a slight increase in mean LDL concentration within the arterial wall. However, if the permeability of the endothelium to LDL was allowed to vary with intra-arterial pressure, then the simulations predicted that the uptake of LDL would be enhanced 1.9-2.6 fold at higher pressure. The magnitude of this increase was consistent with experimental data. We conclude that the concentration polarization effects, enhanced by elevated intra-arterial pressure, cannot explain the increase in LDL uptake seen under hypertensive conditions. Instead, the data are most consistent with a pressure-linked increase in endothelial permeability to LDL.
高血压是动脉粥样硬化的一个危险因素，它会增加动脉壁对低密度脂蛋白（LDL）的摄取。我们这项工作的目的是使用计算模型来确定可能部分导致这种效应的物理因素。以耦合方式计算动脉模型管腔和管壁中的流体流动和传质模式，尽可能紧密地复制先前的实验研究，在这些实验中，在直的、切除的动脉段中测量LDL进入动脉壁的情况。在有血流和无血流的条件下，模拟预测当动脉压从120 mmHg升高到160 mmHg时，动脉壁处LDL的浓度极化会增加。然而，这仅导致动脉壁内平均LDL浓度略有增加。但是，如果允许内皮对LDL的通透性随动脉内压变化，那么模拟预测在较高压力下LDL的摄取将增强1.9 - 2.6倍。这种增加的幅度与实验数据一致。我们得出结论，动脉内压升高所增强的浓度极化效应无法解释高血压条件下所见的LDL摄取增加。相反，数据与内皮对LDL的通透性随压力相关增加最为一致。
