Modeling cerebral network hemodynamics: Effect of conducted vasodilation on brain perfusion.

Neuronal activity signals local changes in functional hyperemia which match metabolic demands for oxygen (O 2 ) ‐and other nutrients, referred to as Neurovascular Coupling (NVC). NVC is essential for proper functioning of the brain and is impaired in various clinical conditions including Alzheimer’s disease, stroke and aging. The emerging paradigm is that neurons and astrocytes release vasoactive mediators in the perivascular space of penetrating arterioles to increase their diameter and blood supply. Recent evidence supports the concept that NVC mediators initiate electrical vasoactive signaling on arterioles that propagate upstream to cause dilation and increase local blood flow. How electrical conduction of neuronal activity along the vasculature shapes the hyperemic response has not been elucidated. In this study, we model hemodynamic responses by conservation of flow, Fahraeus–Lindqvist effect, and the phase separation. Simulations are performed in macroscale reconstructed brain vascular networks. The model examines changes in tissue perfusion in response to neuronal activity and predicts the requirements for propagating electrical signals to evoke physiologically relevant changes in blood perfusion. The theoretical framework presented allows for testing proposed NVC mechanisms and assisting in the interpretation of macroscale functional imaging responses in health and in disease.