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Updated: Jul 11, 2025

In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
Published on: November 3, 2015
The directional flow generated by peristalsis in perivascular networks-Theoretical and numerical reduced-order
I G Gjerde1, M E Rognes1, A L Sánchez2
1Department of Numerical Analysis and Scientific Computing, Simula Research Laboratory, Kristian Augusts gate 23, Oslo 0164, Norway.
Abstract:
Directional fluid flow in perivascular spaces surrounding cerebral arteries is hypothesized to play a key role in brain solute transport and clearance. While various drivers for a pulsatile flow, such as cardiac or respiratory pulsations, are well quantified, the question remains as to which mechanisms could induce a directional flow within physiological regimes. To address this question, we develop theoretical and numerical reduced-order models to quantify the directional (net) flow induceable by peristaltic pumping in periarterial networks. Each periarterial element is modeled as a slender annular space bounded internally by a circular tube supporting a periodic traveling (peristaltic) wave. Under reasonable assumptions of a small Reynolds number flow, small radii, and small-amplitude peristaltic waves, we use lubrication theory and regular perturbation methods to derive theoretical expressions for the directional net flow and pressure distribution in the perivascular network. The reduced model is used to derive closed-form analytical expressions for the net flow for simple network configurations of interest, including single elements, two elements in tandem, and a three element bifurcation, with results compared with numerical predictions. In particular, we provide a computable theoretical estimate of the net flow induced by peristaltic motion in perivascular networks as a function of physiological parameters, notably, wave length, frequency, amplitude, and perivascular dimensions. Quantifying the maximal net flow for specific physiological regimes, we find that vasomotion may induce net pial periarterial flow velocities on the order of a few to tens of m/s and that sleep-related changes in vasomotion pulsatility may drive a threefold flow increase.
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