(460b) Cross-Stream Distribution and Dynamics of Red Blood Cells in Sickle Cell Disease | AIChE

(460b) Cross-Stream Distribution and Dynamics of Red Blood Cells in Sickle Cell Disease


Zhang, X. - Presenter, University of Wisconsin-Madison
Graham, M., University of Wisconsin-Madison
Both experimental and computational studies have shown that in normal blood flow, red blood cells (RBCs) tend to migrate away from the vessel walls, leaving a RBC-depleted region (called the “cell-free layer”) near the walls, while leukocytes and platelets, in contrast, tend to aggregate near the vessel walls, a phenomenon known as “margination”. This segregation behavior of different cellular components in blood flow can be driven by their differences in stiffness and shape. An alteration of this scenario may provide a pathological mechanism for endothelial dysfunction, which is often associated with sickle cell disease (SCD). We hypothesize that in SCD, the sickle RBCs, which are considerably stiffer than the healthy RBCs, may marginate towards the vessel walls and exert repeated damage to the endothelium, causing endothelial dysfunction as a consequence. Direct numerical simulations are performed using an accelerated boundary integral method to study flowing suspensions subjected to pressure-driven flow in a planar slit containing a binary mixture of deformable biconcave discoids and stiff curved prolate spheroids, or sickles, that represent healthy and sickle RBCs, respectively. The key observation in such suspensions is that the sickles exhibit a strong margination towards the walls. The deformable biconcave discoids tend to undergo a so-called tank-treading motion, while the stiff sickles behave like rigid bodies and undergo a Jeffery-like tumbling or kayaking motion. A systematic investigation of the dynamics of single sickles in free and confined shear flows further reveals that the steady-state motion of the sickles is independent of their initial orientations. The margination behavior coupled with the Jeffery-like motions of the sickles near the walls may help substantiate the aforementioned hypothesis of the mechanism for the SCD complications.