Cerebral autoregulation plays a key physiological role by limiting bloodflow changes in the face of pressure fluctuations. Although the underlying vascular cellular processes are chemo-mechanically driven, estimating...
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Cerebral autoregulation plays a key physiological role by limiting bloodflow changes in the face of pressure fluctuations. Although the underlying vascular cellular processes are chemo-mechanically driven, estimating the associated haemodynamic forces in vivo remains extremely difficult and uncertain. In this work, we propose a novel computational methodology for evaluating the bloodflowdynamics across networks of myogenically-active cerebral arteries, which can modulate their muscular tone to stabilize flow (and perfusion pressure) as well as to limit vascular intramural stress. The introduced framework integrates a continuum mechanics-based, biologically-motivated model of the rat vascular wall with 1d blood flow dynamics. We investigate the time dependency of the vascular wall response to pressure changes at both single vessel and network levels. The dynamical performance of the vessel wall mechanics model was validated against different pressure protocols and conditions (control and absence of extracellular Ca2+). The robustness of the integrated fluid–structure interaction framework was assessed using different types of inlet signals and numerical settings in an idealized vascular network formed by a middle cerebral artery and its three generations. The proposed in-silico methodology aims to quantify how acute changes in upstream luminal pressure propagate and influence bloodflow across a network of rat cerebral arteries. Weak coupling ensured accurate results with a lower computational cost for the vessel size and boundary conditions considered. To complete the analysis, we evaluated the effect of an upstream pressure surge on vascular network haemodynamics in the presence and absence of myogenic tone. This provided a clear quantitative picture of how pressure, flow and vascular constriction are re-distributed across each vessel generation upon inlet pressure changes. This work paves the way for future combined experimental-computational studies aiming to
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