Shear stress and intravascular pressure effects on vascular dynamics: two-phase blood flow in elastic microvessels accounting for the passive stresses

Abstract

We study the steady hemodynamics in physiological elastic microvessels proposing an advanced fluid-structure interaction model. The arteriolar tissue is modeled as a two-layer fiber-reinforced hyperelastic material representing its Media and Adventitia layers. The constitutive model employed (Holzapfel et al. in J Elast 61:1-48, 2000) is parametrized via available data on stress-strain experiments for arterioles. The model is completed by simulating the blood/plasma flow in the lumen, using the thixotropic elasto-viscoplastic model in its core, and the linear Phan-Thien and Tanner viscoelastic model in its annular part. The Cell-Free Layer (CFL) and the Fåhraeus and Fåhraeus-Lindqvist effects are considered via analytical expressions based on experimental data (Giannokostas et al. in Materials (Basel) 14:367, 2021b). The coupling between tissue deformation and blood flow is achieved through the experimentally verified pressure-shear hypothesis (Pries et al. Circ Res 77:1017-1023, 1995). Our calculations confirm that the increase in the reference inner radius produces larger expansion. Also, by increasing the intraluminal pressure, the thinning of the walls is more pronounced and it may reach 40% of the initial thickness. Comparing our predictions with those in rigid-wall microtubes, we conclude that apart from the vital importance of vasodilation, there is an up to 25% reduction in wall shear stress. The passive vasodilation contributes to the decrease in the tissue stress fields and affects the hemodynamic features such as the CFL thickness, reducing the plasma layer when blood flows in vessels with elastic walls, in quantitative agreement with previous experiments. Our calculations verify the correctness of the pressure-shear hypothesis but not that of the Laplace law.

Keywords: Blood flow; Blood thixotropy; Blood viscoelasticity; Cell-free layer; Elastic microvessels; Media & adventitia layers; Vasodilation; Wall anisotropy.