| Summary: | Objective: Ischaemic stroke is a leading cause of death and disability. Autoregulation and collateral blood flow through the circle of Willis both play a role in preventing tissue infarction. To investigate the interaction of these mechanisms a one-dimensional steady state model of the cerebral arterial network was created. Methods: Structural variants of the circle of Willis that present particular risk of stroke were recreated using a network model coupled with: (1) a steady state physiological model of cerebral autoregulation; (2) one wherein the cerebral vascular bed was modelled as a passive resistance. Simulations were performed in various conditions of internal carotid and vertebral artery occlusion. Results: Collateral flow alone is unable to ensure adequate blood flow (> 90% normal flow) to the cerebral arteries in several common variants during internal carotid artery occlusion. However, compared to a passive model, cerebral autoregulation is better able to exploit available collateral flow and to maintain flows within 10% of baseline. This is true for nearly all configurations. Conclusion: Hence, autoregulation is a crucial facilitator of collateral flow through the circle of Willis. Significance: Impairment of this response during ischemia will severely impact cerebral blood flows, and tissue survival, and hence autoregulation should be monitored in this situation.
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