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Fig. 3 | Fluids and Barriers of the CNS

Fig. 3

From: Functional hyperemia drives fluid exchange in the paravascular space

Fig. 3

Arteriolar pulsation-driven flow in the PVS in an arteriolar-brain model with realistic mechanical properties. Note the geometry is depicted with an unequal aspect ratio in the radial (r) and axial (z) directions for viewing convenience. a The model of the penetrating arteriole. The brain tissue is modelled as a compliant solid. The subarachnoid space is modelled as a flow resistance (Rs) at the pial end of the PVS and the parenchyma is modelled as a flow resistance (Rp) at the other end. For the simulation with the subarachnoid space modelled as a fluid filled region, see Additional file 7: Fig S5. b A schematic depicting the fluid–structure interaction model described in (a). The arteriolar wall movement drives the fluid movement in the PVS. This fluid movement is coupled with the pressure changes. These pressure changes deform the brain tissue, changing the shape and volume of the PVS. These volume changes will affect the flow in the PVS, as demonstrated in (c). c Plot showing the axial fluid velocity (velocity in the z-direction) in a cross section of the PVS, when the arteriolar wall movement is given by periodic pulsations. The amplitude and frequency of the arteriolar pulsations are taken to be typical values for cerebral arterioles in mice. Fluid velocity vectors (arrows) are provided to help the reader interpret the flow direction from the colors. The region in white has little to no flow. These plots show that there is no appreciable flow into the PVS driven by arteriolar pulsations. Note: Arteriolar and brain tissue displacements induced by arteriolar pulsations are very small (< 0.1 µm). To make the movements clearly visible, we scaled the displacements by a factor of 10 in post-processing. These calculations were performed with fluid permeability, ks = 2 × 10−14 m2 and tissue shear modulus µs = 4 kPa

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