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

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.

Effect of Circadian Rhythm Modulated Blood Flow on Nanoparticle based Targeted Drug Delivery in VirtualIn VivoArterial Geometries

“…Site 2, located at a curvature of the blood vessels, experiences non-uniform shear stress distribution, with areas of lower shear stress typically found on the inner wall of the curve. These areas provide a favorable environment for nanoparticle accumulation due to reduced shear forces acting on the particles, allowing them to remain in contact with the vessel wall for longer periods [ 55 ]. Adhesion at site 1 saturates after 40 seconds, resulting in a plateau in the time evolution plot ( Figure 15A ).…”