Multiphysics Models of Cerebral Blood Flow Regulation
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The cerebral vasculature comprises a highly complex network of blood vessels over a wide range of length scales, from a few micrometres to a few millimetres. The network is both highly connected and highly active in response to changes in both global stimuli (e.g., blood pressure) and local stimuli (e.g., local activation). Changes in the response to blood pressure (the mechanism known as cerebral autoregulation) are implicated in a number of pathological conditions, including stroke, dementia, and traumatic brain injury [1]. However, little work has been performed to consider the active response of the cerebral vasculature in terms of its spatial variability. One model has developed the active response in a network of vessels, but although showing good agreement with experimental data, this model is very computationally expensive [2]. I therefore present work on a new formulation to consider the active response at a whole-brain level using a multiple length scale approach. This is based on a twin feedback model, responding to local changes in both direct and shear stress in the arteriolar bed (manuscript in submission). The model exhibits the characteristic biphasic response but shows that the speed, but not the magnitude, of autoregulation is highly depth dependent. Autoregulation thus seems to be well-preserved at depth, although the response is slower. Results in both a simplified 1D geometry and a full 3D brain geometry will be presented [3], illustrating the importance of considering an accurate geometry. Results will also be presented on how to link network models with compartmental models in this context, using a homogenisation approach. This will be important in extending the model to other forms of cerebral blood flow control, such as cerebrovascular reactivity and the neurovascular coupling, both of which are also impaired in multiple clinical conditions. These whole-brain models of regulation of cerebral blood flow will be valuable in providing a better understanding of the mechanisms that drive this control, and hence in targeting their impairment in pathological conditions.