Viscoelastic Coupling of Pulsatile Wall Shear Stress and Endothelial Glycocalyx Mechanotransduction: A Non-Equilibrium Hydrodynamic Model for Microvascular Resilience

Abstract

The endothelial glycocalyx layer (EGL) functions as the primary mechanosensitive interface modulating hemodynamic forces at the vascular wall [1, 2]. Under physiological pulsatile flow, the transmission of wall shear stress (WSS) to the underlying endothelial cytoskeleton is mediated by the viscoelastic behavior of the EGL porous meshwork [2, 3]. We present a non-equilibrium hydrodynamic framework coupling Brinkman-extended momentum transport with a fractional viscoelastic constitutive model of the EGL core proteoglycans [4, 5]. By solving the coupled fluid-porous matrix equations under dynamic, time-harmonic pressure gradients, we quantify the frequency-dependent attenuation and phase lag of shear forces transmitted to the plasma membrane [1, 6].

Our analytical and numerical solutions reveal that the non-equilibrium viscoelastic relaxation of the glycocalyx acts as a low-pass biophysical filter, shielding endothelial membrane domains from peak high-frequency oscillatory stresses while sustaining baseline mechanotransductive signaling (e.g., eNOS phosphorylation at Ser1177) [2, 7]. Integrating Shannon channel capacity and thermodynamic noise reduction principles from the Science

4.0 framework [8, 9], we demonstrate that preserving the structural elasticity and thickness of the EGL minimizes viscous energy dissipation (E_diss) and prevents non-linear transitions toward endothelial dysfunction [10, 11]. Degradation of the EGL alters this hydrodynamic damping, shifting the mechanotransduction regime toward unbuffered mechanical fatigue, microvascular stasis, and systemic barrier failure [3, 12].