Abstract
Capillary blood vessels, the smallest vessels in the body, form an intricate network with constantly bifurcating, merging and winding vessels. Red blood cells (RBCs) must navigate through such complex microvascular networks in order to maintain tissue perfusion and oxygenation. Normal, healthy RBCs are extremely deformable and able to easily flow through narrow vessels. However, RBC deformability is reduced in many pathological conditions and during blood storage. The influence of reduced cell deformability on microvascular hemodynamics is not well established. Here we use a high-fidelity, 3D computational model of blood flow that retains exact geometric details of physiologically realistic microvascular networks, and deformation of every one of nearly a thousand RBCs flowing through the networks. We predict that reduced RBC deformability alters RBC trafficking with significant and heterogeneous changes in hematocrit. We quantify such changes along with RBC partitioning and lingering at vascular bifurcations, perfusion and vascular resistance, and wall shear stress. We elucidate the cellular-scale mechanisms that cause such changes. We show that such changes arise primarily due to the altered RBC dynamics at vascular bifurcations, as well as cross-stream migration. Less deformable cells tend to linger less at majority of bifurcations increasing the fraction of RBCs entering the higher flow branches. Changes in vascular resistance also seen to be heterogeneous and correlate with hematocrit changes. Furthermore, alteration in RBC dynamics is shown to cause localized changes in wall shear stress within vessels and near vascular bifurcations. Such heterogeneous and focal changes in hemodynamics may be the cause of morphological abnormalities in capillary vessel networks as observed in several diseases.
Highlights
Capillary blood vessels, the smallest vessels in the body, form an intricate network with constantly bifurcating, merging and winding vessels
Heterogeneous distribution of Red blood cells (RBCs) which is a hallmark of microvascular blood flow in vivo is observed across each simulated network as some capillary vessels are seen to be filled with cells, while some vessels are sparsely populated
To predict blood flow in microvascular networks, previous theoretical models have often used 1D network flow models[61,62,69]. While such models allow consideration of large microvascular networks comprised of many blood vessels, they treat individual vessel as 1D segments
Summary
The smallest vessels in the body, form an intricate network with constantly bifurcating, merging and winding vessels. Shown that cellular-scale phenomena dictate RBC distribution in the network These include, among others, the lingering behavior of an individual RBC at a capillary bifurcation where the cell can stretch significantly and reside near the stagnation-point longer than a freely flowing c ell[18–23], and a radially skewed hematocrit profile over a vessel cross-section caused by the presence of upstream bifurcations[14,17,22–26]. Many pathological conditions, such as sickle cell disease, malaria, diabetes mellitus, and sepsis, are associated with a loss of RBC deformability[27–34]. Hypoxiamediated NO release from RBC-bound hemoglobin was shown to diminish under hyperglycemia[57,58]
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