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Simulation of metabolic blood flow regulation in heterogeneous microvascular networks: Effects of hematocrit variations

A theoretical model is presented for simulating oxygen transport and blood flow regulation in microvascular networks with realistic heterogeneous structures. The distribution of flow and hematocrit is predicted using a model for microvessel hemodynamics, including unequal hematocrit partition at diverging vessel bifurcations. Flow regulation is modeled based on length‐tension characteristics of vascular smooth muscle, and includes myogenic, shear‐dependent and metabolic responses. If the metabolic signal is assumed to originate solely from a red‐blood‐cell‐dependent mechanism, the model predicts unrealistic behavior in two respects. Firstly, a reduction in systemic hematocrit causes a decrease in flow, rather than an increase as expected. Secondly, low flow channels receive a low hematocrit and generate a reduced metabolic signal, causing further flow reduction and leading to uneven oxygenation with hypoxia in some flow channels. These findings suggest that some other mechanism, not dependent on red blood cells, must contribute to metabolic flow regulation. Inclusion in the model of a wall‐derived signal dependent on local oxygen level leads to higher flow in response to hematocrit reduction and more uniform distributions of blood flow and tissue oxygenation. Supported by NIH grant HL070657.