Speaker
Description
Cerebral autoregulation stabilizes cerebral blood flow despite changes in blood pressure through adjustments in arterial diameter. However, the precise roles of individual vessels and impaired autoregulation in outcomes after ischemic stroke remain poorly understood. We present a computational framework incorporating static myogenic and endothelial regulation in large semi-realistic microvascular networks derived from mouse cortical vasculature (~200,000 vessels). Arteries actively regulate their diameter, whereas capillaries and veins behave passively according to a pressure–area relationship. Changes in transmural pressure and shear stress modulate vascular wall stiffness and compliance, enabling active arterial diameter adaptation and linking local haemodynamic stimuli to vessel-level flow regulation. Autoregulatory responses were evaluated under three conditions: healthy regulation, post-occlusion reperfusion with altered vascular reactivity, and chronic autoregulatory dysfunction. Under healthy conditions, the simulations reveal the dominant role of surface arteries in buffering pressure changes. During reperfusion, impaired myogenic reactivity emerges as a key driver of post-stroke hyperperfusion. Progressive loss of autoregulation in arteries within the previously ischemic territory disrupts capillary perfusion. These results provide mechanistic insight into how microvascular structure and vessel-level regulation shape cerebral perfusion in health and after stroke.
