Red Blood Cell‐resolved 3D Computational Modeling of Blood Flow in Physiologically Realistic Microvascular Networks

Abstract

Microvascular networks represent geometrically complex architecture due to constantly bifurcating and merging vessels. Moreover, blood vessels are not necessarily straight, and often highly winding. Mathematical models of blood flow in such networks have treated these vessels as 1D straight segments neglecting the geometric complexity and details. These models also do not consider the deformation and flow of individual red blood cell, and instead use empirical relations to prescribe blood viscosity and red blood cell distribution at a vascular bifurcation. As such, these models cannot predict hemodynamic variations over short time and length scales. To overcome this limitation, we have recently developed a high‐fidelity 3D, first‐principle based, fluid‐‐structure interaction model of blood flow in physiologically realistic microvascular networks. The model retains the exact geometric details of the vasculature, e.g., 3D nature of the blood vessels and bifurcations, and vessel curvature. Deformation and flow of each individual red blood cell as they flow through the vessels are exactly modeled. The model is based on the minimal assumptions: it does not assume any empirical viscosity law or bifurcation law; rather, these laws are predicted by the model. The model provides microscale details of hemodynamic quantities that are not readily available in experiments, and cannot be predicted by the traditional 1D network models, such as wall shear stress gradient and time‐dependent red blood cell partitioning at bifurcations.Of particular interest is the role of red blood cell deformability on hematocrit distribution in the networks. Cell deformability is known to reduce in many diseases, such as sickle cell disease, malaria and diabetes. By using in vivo images of retinal microvasculature, we have performed simulation of network blood flow under varying cell deformability in such networks. The model shows that altered cell deformability significantly changes the cell distribution in the network, and subsequently the flow resistance in vessels. While some vessels show a significant increase in hematocrit, some show a significant decrease. Such a redistribution of hematocrit for diseased red blood cells may have a significant impact on tissue oxygen delivery. The simulation results are used to mechanistically explain the observed redistribution of hematocrit and vascular resistance.Support or Funding InformationFunded by NSF