Abstract
It is well known that the mechanical behavior of arterial walls plays an important role in the pathogenesis of vascular diseases. Most studies existing in the literature focus on the mechanical interactions between the blood flow and wall’s deformations. However, in the brain, the smaller vessels experience not only oscillatory forces due to the pulsatile blood flow but also structural and morphological changes controlled by the surrounding brain cells. In this study, the mechanical deformation of the cerebral arterial wall caused by the pulsatile blood flow and the dynamics of the neuronal nitric oxide (NO) is investigated. NO is a small diffusive gaseous molecule produced by the endothelial cells and neurons, which is involved in the regulation of cerebral blood flow and pressure. The cerebral vessel is assumed to be a hollow axial symmetric cylinder whose wall thickness is much smaller than the cylinder’s radius and longitudinal length is much less than the propagating wavelength. The wall is an isotropic, homogeneous linear viscoelastic material described by an NO-modulated variable-order fractional Maxwell model. A fractional telegraph equation is obtained for the axial component of the displacement. Patterns of wall’s deformation are investigated through numerical simulations. The results suggest that a significantly decreased inactivation of the neuronal NO may cause a reduction in the shear stress at the blood-vessel interface, which could lead to a decrease in the production of shear-induced endothelial NO and neurovascular disease.
Highlights
Cerebral vasculature plays a critical role in brain’s metabolism and neurovascular conditions
A small diffusive gaseous molecule, the nitric oxide (NO)-Modulated Viscoelastic Model of Vessels cerebral NO is mainly produced by shear-induced mechanotransduction at the blood-vessel interface (Sriram et al, 2016) and by synthesis reactions within the endothelial cells of the blood vessels and neurons (Forstermann and Sessa, 2012)
While the cerebral NO activity causes the local vasodilatation of downstream cerebral vessels at the neuroglial-vascular unit site, the NO diffusion within the vascular wall relaxes the smooth muscle cells leading to the so-called remote vasodilation due to the propagation of muscle’s relaxation to the upstream arteries via the intercellular communications among endothelial and smooth muscle cells (Freed and Gutterman, 2017) facilitated by vascular gap junctions (Iadecola, 2004; Iadecola, 2017)
Summary
Cerebral vasculature plays a critical role in brain’s metabolism and neurovascular conditions. It is acknowledged that the neurons and glial cells control the cerebral blood flow through the chemo-mechanical activation of the cells within the vascular wall (Attwell et al, 2010). The regulation of the blood flow in brain is achieved through vasomotor mechanisms in which both the neuronal and endothelial NO are involved (Cockcroft, 2005; Metea and Newman, 2006; Attwell et al, 2010; Atochin and Huang, 2011; Petzold and Murthy, 2011; Contestabile et al, 2012; Lourenco et al, 2014; Haselden et al, 2020). Impaired cerebral NO production and/or decay can signal the presence of a neurovascular disease (Parker and Parks, 1995; Maurer et al, 2000; Wilkinson et al, 2004; Unitt et al, 2010; Santos et al, 2011; Haselden et al, 2020)
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