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血管壁几何形状对红细胞壁诱导迁移的影响。

Influence of the vessel wall geometry on the wall-induced migration of red blood cells.

机构信息

Department of Mathematics, Brandeis University, Waltham, Massachusetts, United States of America.

出版信息

PLoS Comput Biol. 2023 Jul 17;19(7):e1011241. doi: 10.1371/journal.pcbi.1011241. eCollection 2023 Jul.

DOI:10.1371/journal.pcbi.1011241
PMID:37459356
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10374106/
Abstract

The geometry of the blood vessel wall plays a regulatory role on the motion of red blood cells (RBCs). The overall topography of the vessel wall depends on many features, among which the endothelial lining of the endothelial surface layer (ESL) is an important one. The endothelial lining of vessel walls presents a large surface area for exchanging materials between blood and tissues. The ESL plays a critical role in regulating vascular permeability, hindering leukocyte adhesion as well as inhibiting coagulation during inflammation. Changes in the ESL structure are believed to cause vascular hyperpermeability and entrap immune cells during sepsis, which could significantly alter the vessel wall geometry and disturb interactions between RBCs and the vessel wall, including the wall-induced migration of RBCs and the thickening of a cell-free layer. To investigate the influence of the vessel wall geometry particularly changed by the ESL under various pathological conditions, such as sepsis, on the motion of RBCs, we developed two models to represent the ESL using the immersed boundary method in two dimensions. In particular, we used simulations to study how the lift force and drag force on a RBC near the vessel wall vary with different wall thickness, spatial variation, and permeability associated with changes in the vessel wall geometry. We find that the spatial variation of the wall has a significant effect on the wall-induced migration of the RBC for a high permeability, and that the wall-induced migration is significantly inhibited as the vessel diameter is increased.

摘要

血管壁的几何形状对红细胞(RBC)的运动起着调节作用。血管壁的整体形貌取决于许多特征,其中内皮表面层(ESL)的内皮衬里是一个重要特征。血管壁的内皮衬里为血液和组织之间的物质交换提供了一个很大的表面积。ESL 在调节血管通透性、阻止白细胞黏附和抑制炎症期间的凝血方面起着关键作用。据信,ESL 结构的变化会导致败血症期间血管通透性增加和免疫细胞被捕获,这可能会显著改变血管壁的几何形状,并扰乱 RBC 与血管壁之间的相互作用,包括 RBC 受壁诱导的迁移和无细胞层的增厚。为了研究 ESL 特别改变的血管壁几何形状在各种病理条件下(如败血症)对 RBC 运动的影响,我们使用浸入边界方法在二维空间中开发了两个模型来表示 ESL。特别是,我们使用模拟来研究在不同的壁厚度、空间变化和与血管壁几何形状变化相关的渗透性下,靠近血管壁的 RBC 上的升力和阻力如何变化。我们发现,对于高渗透性,壁的空间变化对 RBC 受壁诱导的迁移有显著影响,并且随着血管直径的增加,壁诱导的迁移显著受到抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/3a359ddd7c42/pcbi.1011241.g018.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/a9c07855c4f8/pcbi.1011241.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/4a4ed282dd47/pcbi.1011241.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/628ecc770da7/pcbi.1011241.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/7bbf48eae827/pcbi.1011241.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/7462ae6f6541/pcbi.1011241.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/8ef4437315f2/pcbi.1011241.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/48e18aec099c/pcbi.1011241.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/e089cfcafe49/pcbi.1011241.g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/02ac1e1dd8b3/pcbi.1011241.g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/f6f9cdc18e56/pcbi.1011241.g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/1317f811fa0a/pcbi.1011241.g015.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/22fc7acac6e0/pcbi.1011241.g016.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/2f4c7f8b651e/pcbi.1011241.g017.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/3a359ddd7c42/pcbi.1011241.g018.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/aaa98fda99c4/pcbi.1011241.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/cc50fda8da14/pcbi.1011241.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/618e289e69fa/pcbi.1011241.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/2c7d4cbf7d83/pcbi.1011241.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/a9c07855c4f8/pcbi.1011241.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/4a4ed282dd47/pcbi.1011241.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/628ecc770da7/pcbi.1011241.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/7bbf48eae827/pcbi.1011241.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/7462ae6f6541/pcbi.1011241.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/8ef4437315f2/pcbi.1011241.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/48e18aec099c/pcbi.1011241.g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/e089cfcafe49/pcbi.1011241.g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/02ac1e1dd8b3/pcbi.1011241.g013.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/f6f9cdc18e56/pcbi.1011241.g014.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/1317f811fa0a/pcbi.1011241.g015.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/22fc7acac6e0/pcbi.1011241.g016.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/2f4c7f8b651e/pcbi.1011241.g017.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cdb/10374106/3a359ddd7c42/pcbi.1011241.g018.jpg

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