MODELING COUPLED DIAMETER AND HEMODYNAMIC OSCILLATIONS IN ARTERIOLAR NETWORKS

Abstract

Regulation of convective O2 supply to capillary beds in organs is accomplished by coordinated changes in upstream arteriolar diameter. To study this regulation system, in vivo experiments have been performed using a gas exchange chamber to sinusoidally oscillate the O2 environment at the surface of a rat skeletal muscle. Capillary hematocrit (H) changes were delayed by several seconds relative to changes in red cell velocity (V) and the delay varied with the animal suggesting geometry dependence. To assess how alterations in diameters led to observed hemodynamics, a computational model was developed that couples variations in network blood flow to conducted diameter changes. The model uses an arteriolar tree that was constructed based on measured data in rat skeletal muscle and a two‐phase (red cells and plasma) time‐dependent model of microvascular blood flow. The initial response to imposed surface O2 oscillations was simulated by applying diameter oscillations at the distal ends of selected terminal arterioles. The model was used to calculate hemodynamic oscillations in the network and, in particular, examine how the transit time for red cells in the network could lead to the observed delay in changes in H relative to those in V. Initial results show similarities to experimental observations, including decreases in hemodynamic response amplitude with increases in forcing frequency and a delay in H relative to V.