scholarly journals A Nitric Oxide–Modulated Variable-Order Fractional Maxwell Viscoelastic Model of Cerebral Vascular Walls

2021 ◽  
Vol 7 ◽  
Author(s):  
Corina S. Drapaca

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.

2006 ◽  
Vol 175 (4S) ◽  
pp. 521-521
Author(s):  
Motoaki Saito ◽  
Tomoharu Kono ◽  
Yukako Kinoshita ◽  
Itaru Satoh ◽  
Keisuke Satoh

2007 ◽  
Vol 55 (S 1) ◽  
Author(s):  
W Schiller ◽  
K Spiegel ◽  
T Schmid ◽  
H Rudorf ◽  
S Flacke ◽  
...  

2020 ◽  
Vol 82 (5) ◽  
pp. 617-625
Author(s):  
Pramod Kumar Yadav ◽  
Bhupesh Dutt Sharma ◽  
A. N. Filippov

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom

Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1175-1182 ◽  
Author(s):  
María Isabel Madrid ◽  
Miguel García-Salom ◽  
Jerónimo Tornel ◽  
Marc de Gasparo ◽  
Francisco J. Fenoy

1996 ◽  
Vol 270 (5) ◽  
pp. H1696-H1703 ◽  
Author(s):  
D. Mitchell ◽  
K. Tyml

Nitric oxide (NO) has been shown to be a potent vasodilator released from endothelial cells (EC) in large blood vessels, but NO release has not been examined in the capillary bed. Because the capillary bed represents the largest source of EC, it may be the largest source of vascular NO. In the present study, we used intravital microscopy to examine the effect of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on the microvasculature of the rat extensor digitorum longus muscle. L-NAME (30 mM) applied locally to a capillary (300 micron(s) from the feeding arteriole) reduced red blood cell (RBC) velocity [VRBC; control VRBC = 238 +/- 58 (SE) micron/s; delta VRBC = -76 +/- 8%] and RBC flux (4.4 +/- 0.7 to 2.8 +/- 0.7 RBC/s) significantly in the capillary, but did not change feeding arteriole diameter (Dcon = 6.3 +/- 0.7 micron, delta D = 5 +/- 7%) or draining venule diameter (Dcon = 10.1 +/- 0.6 micron, delta D = 4 +/- 2%). Because of the VRBC change, the flux reduction was equivalent to an increased local hemoconcentration from 1.8 to 5 RBCs per 100 micron capillary length. L-NAME also caused an increase in the number of adhering leukocytes in the venule from 0.29 to 1.43 cells/100 micron. L-NAME (30 mM) applied either to arterioles or to venules did not change capillary VRBC. Bradykinin (BK) locally applied to the capillary caused significant increases in VRBC (delta VRBC = 111 +/- 23%) and in arteriolar diameter (delta D = 40 +/- 5%). This BK response was blocked by capillary pretreatment with 30 mM L-NAME (delta VRBC = -4 +/- 27%; delta D = 5 +/- 9% after BK). We concluded that NO may be released from capillary EC both basally and in response to the vasodilator BK. We hypothesize that 1) low basal levels of NO affect capillary blood flow by modulating local hemoconcentration and leukocyte adhesion, and 2) higher levels of NO (stimulated by BK) may cause a remote vasodilation to increase microvascular blood flow.


Dynamics ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 9-17
Author(s):  
Andrea Natale Impiombato ◽  
Giorgio La Civita ◽  
Francesco Orlandi ◽  
Flavia Schwarz Franceschini Zinani ◽  
Luiz Alberto Oliveira Rocha ◽  
...  

As it is known, the Womersley function models velocity as a function of radius and time. It has been widely used to simulate the pulsatile blood flow through circular ducts. In this context, the present study is focused on the introduction of a simple function as an approximation of the Womersley function in order to evaluate its accuracy. This approximation consists of a simple quadratic function, suitable to be implemented in most commercial and non-commercial computational fluid dynamics codes, without the aid of external mathematical libraries. The Womersley function and the new function have been implemented here as boundary conditions in OpenFOAM ESI software (v.1906). The discrepancy between the obtained results proved to be within 0.7%, which fully validates the calculation approach implemented here. This approach is valid when a simplified analysis of the system is pointed out, in which flow reversals are not contemplated.


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