Abstract
Blood flow in sickle cell disease (SCD) can substantially differ from normal blood flow due to significant alterations in the physical properties of the red blood cells (RBCs). Chronic complications, such as inflammation of the endothelial cells lining blood vessel walls, are associated with SCD, for reasons that are unclear. Here, detailed boundary integral simulations are performed to investigate an idealized model flow flow in SCD, a binary suspension of flexible biconcave discoidal fluid-filled capsules and stiff curved prolate capsules that represent healthy and sickle RBCs, respectively, subjected to pressure-driven flow in a planar slit. The stiff component is dilute. The key observation is that, unlike healthy RBCs that concentrate around the center of the channel and form an RBC-depleted layer (i.e. cell-free layer) next to the walls, sickle cells are largely drained from the bulk of the suspension and aggregate inside the cell-free layer, displaying strong margination. These cells are found to undergo a rigid-body-like rolling orbit near the walls. A binary suspension of flexible biconcave discoidal capsules and stiff straight (non-curved) prolate capsules is also considered for comparison, and the curvature of the stiff component is found to play a minor role in the behavior. Additionally, by considering a mixture of flexible and stiff biconcave discoids, we reveal that rigidity difference by itself is sufficient to induce the segregation behavior in a binary suspension. Furthermore, the additional shear stress on the walls induced by the presence of cells is computed for the various cases. Compared to the small fluctuations in wall shear stress for a suspension of healthy RBCs, large local peaks in wall shear stress are observed for the binary suspensions, due to the proximity of the marginated stiff cells to the walls. This effect is most marked for the straight prolate capsules. As endothelial cells are known to mechanotransduce physical forces such as aberrations in shear stress and convert them to physiological processes such as activation of inflammatory signals, these results may aid in understanding mechanisms for endothelial dysfunction associated with SCD.