![]() More symmetric shapes and tumbling motion are expected to reduce the lift velocity. The shape and the mode of particle rotation, namely tank-treading, tumbling, swinging, or breathing motion, are correlated with the lift velocity. It has been shown that the lift velocity generally depends on capillary number Ca (the ratio of viscous forces to the membrane shear elastic forces), the viscosity contrast (λ), and the height of the channel. There is another lift mechanism in pressure driven flows, due to the non-zero curvature of the flow field which drives the cells closer to the center-line, in order to minimize particle deformation. Individual cell migration is partly due to a wall-induced lift force, with the velocity proportional to the stresslet, i.e., the symmetric part of the first moment of particle surface traction and inversely proportional to the squared vertical distance from the walls. Therefore, the local hematocrit of RBCs normal to the vessel walls affects the margination of platelets and their reactions with the endothelial cells in the event of an injury when the clotting cascade begins. In addition, the migration of the red blood cells induces the margination of stiffer platelets. This layer is known to contribute in the reduction of the blood viscosity or plasma skimming as blood perfuses the smaller vessels. The migration of RBCs is of direct biological importance – as the cells move towards the center-line in pressure driven flows, a cell-free layer (CFL) is formed near the vessel walls (also known as Fahraeus-Lindqvist layer). This flexibility, and resulting lift force causes the cells to migrate away from the vessel walls when they are exposed to the blood stream. ![]() Their reduced volume is about 0.65 (, where V is the cell volume and S is its surface area) and are highly flexible. ![]() Red blood cells take up to 45% volume fraction (Hematocrit) in the whole blood and are the oxygen carriers with biconcave shape with equivalent radius of about 2.82 μm. Whole blood is a complex fluid composed of plasma as the suspending medium and three main cellular components: red blood cells (RBCs), platelets and white blood cells. Microcirculation in vascular systems is a vital component of living organisms where oxygenated blood passes through terminal arterioles (smaller blood vessels with 20 to 50 micron diameter) and capillaries (~10 microns). We explain this result by comparing lift and collision trajectories of cells at different viscosity contrasts. Our results also indicate that at a hematocrit of 10% that the viscosity contrast is not negligible when calculating the cell free layer thickness. We show that channel size qualitatively changes how the cells distribute in the channel. We utilize a massively-parallel immersed boundary code coupled to a finite volume solver to capture the particle resolved physics. In this work, we present the results of large-scale simulations that show how the channel size, viscosity contrast of the red blood cells, and hematocrit affect cell distributions and the cell-free layer in these systems. ![]() To date, little progress has been made studying small arteriole flows (20-40 μm) with a hematocrit (red blood cell volume fraction) of 10-20% and a physiological viscosity contrast. However, studying red blood cell flows via computer simulations is challenging due to the complex shapes and the non-trivial viscosity contrast of a red blood cell. The dynamics of red blood cells in small arterioles are important as these dynamics affect many physiological processes such as hemostasis and thrombosis. ![]()
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