The ability of the cerebral vasculature to regulate vascular diameter, hence resistance and cerebral blood flow (CBF), in response to metabolic demands (neurovascular coupling), and perfusion pressure changes (autoregulation) may be assessed by measuring the CBF response to carbon dioxide (CO2 ). In healthy individuals, the CBF response to a ramp CO2 stimulus from hypocapnia to hypercapnia is assumed sigmoidal or linear. However, other response patterns commonly occur, especially in individuals with cerebrovascular disease, and these remain unexplained. CBF responses to CO2 in a vascular region are determined by the combined effects of the innate vascular responses to CO2 and the local perfusion pressure; the latter ensuing from pressure-flow interactions within the cerebral vascular network. We modeled this situation as two vascular beds perfused in parallel from a fixed resistance source. Our premise is that all vascular beds have a sigmoidal reduction of resistance in response to a progressive rise in CO2 . Surrogate CBF data to test the model was provided by magnetic resonance imaging of blood oxygen level-dependent (BOLD) signals. The model successfully generated all the various BOLD-CO2 response patterns, providing a physiological explanation of CBF distribution as relative differences in the network of vascular bed resistance responses to CO2 . Hum Brain Mapp 38:5590-5602, 2017. © 2017 Wiley Periodicals, Inc.
Keywords: carbon dioxide; cerebral blood flow; cerebral vascular resistance; model.
© 2017 Wiley Periodicals, Inc.