Modeling the hemodynamic response due to vasodilatory signals conducted upstream along the arteriolar tree

Abstract

To study local regulation of convective O2 delivery, in vivo experiments were conducted using a gas chamber to oscillate the O2 environment at one surface of rat skeletal muscle. Intravital video microscopy enabled quantification of the hemodynamic (RBC velocity, V, and hematocrit, H) and O2 saturation responses in capillaries. To assess how changes in arteriolar diameters lead to the observed blood flow response, a model of the lower three levels of the arteriolar tree was constructed based on published data. Sinusoidal changes in vessel diameter were imposed at the distal end of one terminal arteriole, and the upstream conduction of these diameter changes was simulated. A quasi‐steady model of two‐phase (RBCs and plasma) blood flow was used to calculate time‐dependent hemodynamics in the network. For a range of forcing frequencies, conduction velocities (Vcond), and attenuation lengths, the ability of the system to control RBC supply in a terminal arteriole was studied. Attenuation lengths within the physiological range (2mm to 2cm) did not affect the flow response. Decreases in frequency and increases in Vcond increased the amplitude of the flow response. For a frequency of 0.025 Hz, varying Vcond from 10 μm/sec to 50 μm/sec increased the RBC supply response by 35%. Predicted changes in H and V showed qualitative agreement with experimental results. Supported by NIH HL‐089125, CIHR to CGE and DG, and NSERC to SJMM.