(311f) Cell Distributions and Segregation during Blood Flow in Sickle Cell Disease and Iron Deficiency Anemia within Straight and Serpentine Vascular Geometries | AIChE

(311f) Cell Distributions and Segregation during Blood Flow in Sickle Cell Disease and Iron Deficiency Anemia within Straight and Serpentine Vascular Geometries

Authors 

Caruso, C., Emory University
Lam, W. A., Georgia Institute of Technology
Graham, M. D., University of Wisconsin-Madison
The spatial distribution of different cellular components of blood is nontrivial. Red blood cells (RBCs) migrate toward the center of blood vessel leaving an RBC-depleted cell-free layer (CFL) near vessel walls, whereas white blood cells and platelets are inclined to reside in these layers, a flow-induced segregation phenomenon called margination. The margination phenomenon may have particular significance in the context of some blood cell disease, such as sickle cell disease (SCD) and iron deficiency anemia (IDA). For instance, a common and important complication of SCD is chronic sickle vasculopathy, in which the endothelial cells that line the blood vessels are dysfunctional and in a pro-inflammatory state in most regions in the circulation. One might hypothesize that diseased cells strongly marginate, residing primarily in the cell-free layer near blood vessel walls, and thereby generating physical interactions such as large shear stress fluctuations and mechanical contacts that damage the endothelium. We study the hematocrit distribution for mixtures of healthy RBCs and iron deficiency RBCs (idRBCs) in straight cylindrical channel using simulations with an immersed boundary method. We find that idRBCs strongly marginate close to channel walls, whereas healthy RBCs tend to enrich around the center of the channel, demonstrating the differences in size and deformability are sufficient to drive segregation behavior. Additionally, to characterize the hydrodynamic effects of the cell distribution on the blood vessel walls, we compute the wall shear stress for binary suspension with idRBCs as well as for a suspension with homogeneous healthy RBCs, which demonstrates that the smaller and stiffer idRBC subpopulations marginate towards the vessel wall causing aberrant shear stresses leads to increased vascular inflammation. Very similar observations arise for mixtures of healthy and irreversibly sickled cells. We also study the effects of geometric complexities of vessels, such as curvature, on cell distribution, and margination phenomena.

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