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首页> 美国卫生研究院文献>Journal of Biomechanical Engineering >Mass Transport of Low Density Lipoprotein in Reconstructed Hemodynamic Environments of Human Carotid Arteries: The Role of Volume and Solute Flux Through the Endothelium
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Mass Transport of Low Density Lipoprotein in Reconstructed Hemodynamic Environments of Human Carotid Arteries: The Role of Volume and Solute Flux Through the Endothelium

机译：低密度脂蛋白在人类颈动脉重建血流动力学环境中的大量运输：通过内皮细胞的体积和溶质通量的作用

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The accumulation of low density lipoprotein (LDL) in the arterial intima is a critical step in the initiation and progression of atheromatous lesions. In this study we examine subject-specific LDL transport into the intima of carotid bifurcations in three human subjects using a three-pore model for LDL mass transfer. Subject-specific carotid artery computational models were derived using magnetic resonance imaging (MRI) to obtain the geometry and phase-contract MRI (PC-MRI) to acquire pulsatile inflow and outflow boundary conditions for each subject. The subjects were selected to represent a wide range of anatomical configurations and different stages of atherosclerotic development from mild to moderate intimal thickening. A fluid–solid interaction (FSI) model was implemented in the computational fluid dynamics (CFD) approach in order to consider the effects of a compliant vessel on wall shear stress (WSS). The WSS-dependent response of the endothelium to LDL mass transfer was modeled by multiple pathways to include the contributions of leaky junctions, normal junctions, and transcytosis to LDL solute and plasma volume flux from the lumen into the intima. Time averaged WSS (TAWSS) over the cardiac cycle was computed to represent the spatial WSS distribution, and wall thickness (WTH) was determined from black blood MRI (BBMRI) so as to visualize intimal thickening patterns in the bifurcations. The regions which are exposed to low TAWSS correspond to elevated WTH and higher mass and volume flux via the leaky junctions. In all subjects, the maximum LDL solute flux was observed to be immediately downstream of the stenosis, supporting observations that existing atherosclerotic lesions tend to progress in the downstream direction of the stenosis.
机译：低密度脂蛋白（LDL）在动脉内膜中的积累是动脉粥样硬化病变开始和发展的关键步骤。在这项研究中，我们使用LDL质量转移的三孔模型检查了三名人类受试者中特定于LDL的运输进入颈动脉分叉内膜的过程。使用磁共振成像（MRI）得出特定于受试者的颈动脉计算模型，以获取几何形状，并利用相位收缩MRI（PC-MRI）来获取每个受试者的搏动性流入和流出边界条件。选择对象以代表从轻度到中度内膜增厚的各种解剖结构和动脉粥样硬化发展的不同阶段。为了考虑顺应性容器对壁切应力（WSS）的影响，在计算流体动力学（CFD）方法中实施了流固耦合（FSI）模型。通过多种途径模拟内皮对LDL传质的WSS依赖性反应，包括渗漏连接，正常连接和胞吞作用对LDL溶质和从内腔进入内膜的血浆体积通量的贡献。计算整个心动周期的时间平均WSS（TAWSS）以表示空间WSS分布，并根据黑血MRI（BBMRI）确定壁厚（WTH），以可视化分叉处的内膜增厚模式。暴露于低TAWSS的区域对应于WTH升高以及通过泄漏连接处更高的质量和体积通量。在所有受试者中，观察到最大的LDL溶质通量位于狭窄的下游，这支持现有的动脉粥样硬化病变倾向于在狭窄的下游方向发展的观察。

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