Blood Flow-Induced Remodeling of the Artery Wall

Author(s):  
B. Lowell Langille
Keyword(s):  
2012 ◽  
Vol 302 (6) ◽  
pp. H1330-H1339 ◽  
Author(s):  
Virginie Bolduc ◽  
Edward Baraghis ◽  
Natacha Duquette ◽  
Nathalie Thorin-Trescases ◽  
Jean Lambert ◽  
...  

Endothelial dysfunction and oxidative stress contribute to the atherosclerotic process that includes stiffening of large peripheral arteries. In contrast, our laboratory previously reported a paradoxical increase in cerebrovascular compliance in LDLr−/−:hApoB+/+ atherosclerotic (ATX) mice ( 7 ). We hypothesized that prevention of cerebral artery endothelial dysfunction with a chronic dietary antioxidant intake would normalize the changes in cerebral artery wall structure and biomechanics and prevent the decline in basal cerebral blood flow associated with atherosclerosis. Three-month-old ATX mice were treated, or not, for 3 mo with the polyphenol (+)-catechin (CAT; 30 mg·kg−1·day−1) and compared with wild-type controls. In isolated, pressurized cerebral arteries from ATX mice, CAT prevented endothelial dysfunction (deterioration of endothelium-dependent, flow-mediated dilations; P < 0.05), the inward hypertrophic structural remodeling (increase in the wall-to-lumen ratio; P < 0.05), and the rise in cerebrovascular compliance (rightward shift of the stress-strain curve measured in passive conditions, reflecting mechanical properties of the arterial wall; P < 0.05). Doppler optical coherence tomography imaging in vivo confirmed these findings, showing that cerebral compliance was higher in ATX mice and normalized by CAT ( P < 0.05). CAT also prevented basal cerebral hypoperfusion in ATX mice ( P < 0.05). Active remodeling of the cerebrovascular wall in ATX mice was further suggested by the increase ( P < 0.05) in pro-metalloproteinase-9 activity, which was normalized by CAT. We conclude that, by preserving the endothelial function, a chronic treatment with CAT prevents the deleterious effect of severe dyslipidemia on cerebral artery wall structure and biomechanical properties, contributing to preserving resting cerebral blood flow.


2008 ◽  
Vol 20 (9) ◽  
pp. 21
Author(s):  
L. A. Vodstrcil ◽  
J. Novak ◽  
M. Tare ◽  
M. E. Wlodek ◽  
L. J. Parry

During pregnancy, the uteroplacental circulation undergoes dramatic alterations to allow for the large increase in blood flow to the feto-placental unit. These alterations are achieved through several mechanisms including structural changes in the uterine artery wall and endothelium-dependent vasodilation. Small renal arteries of relaxin-deficient mice and rats have enhanced myogenic reactivity and decreased passive compliance, and are relatively vasoconstricted (Novak et al. 2001, 2006). To date, no study has identified relaxin receptors (Rxfp1) in arteries or investigated the effects of relaxin deficiency in pregnancy on uterine artery function. The aims of this current study were to: 1) localise Rxfp1 in the uterine arteries, 2) measure myogenic reactivity in small uterine arteries after relaxin treatment, and 3) test the hypothesis that blocking circulating relaxin in late pregnancy will increase uterine artery wall stiffness. We demonstrated that Rxfp1 is expressed in the uterine arteries of pregnant mice and rats. Brightfield immunohistochemistry and immunofluorescence using antibodies specific for rat Rxfp1, α-smooth muscle actin and CD31 localised Rxfp1 protein predominantly to the vascular smooth muscle in the uterine artery of pregnant rats. Administration of recombinant human H2 relaxin (4 ug/h) for 6 h or 5 days in intact and ovariectomised rats reduced myogenic reactivity of small uterine arteries in vitro. Pregnant rats were treated with a monoclonal antibody against circulating relaxin (MCA1) or control (MCAF) for 3 days (Days 17–19) and uterine arteries were mounted on a pressure myograph to assess passive mechanical wall properties. Neutralising circulating relaxin in late pregnancy resulted in a significant increase in uterine artery wall stiffness. These data demonstrate that relaxin acts on the vascular smooth muscle cells in the uterine artery and may be involved in the pregnancy-specific vascular remodelling of uterine arteries to increase vasodilation and blood flow to the uterus and placenta. (1) Novak J et al. (2001). J Clin Invest 107: 1469–75 (2) Novak J et al. (2006). FASEB J 20: 2352–62


Author(s):  
M. A. Al-Rawi ◽  
A. M. Al-Jumaily ◽  
A. Lowe

Non-invasive diagnosis of cardiovascular diseases is a valuable tool to reduce patient’s risk and discomfort. The main aim of this work is to investigate the possibilities of using computational fluid dynamics as a tool to investigate the biomechanical characteristics of the aorta under different medical conditions. These conditions include an aorta with healthy conditions, atherosclerosis and aneurysm. A three dimensional pulsatile flow model for an elastic aorta is developed and constructed in ANSYS® CFX 12. Abnormalities are simulated as diameter changes at the root of the ascending aorta. The computational model shows the reflection of these diseases on the blood flow and the artery wall at other locations downstream along the aorta. This 3D model has several advantages over previously published 1D and 2D models by giving more realistic results as compared with clinical trials.


2015 ◽  
Vol 4 (1-2) ◽  
pp. 38-42 ◽  
Author(s):  
Gelin Xu ◽  
Xinying Fan ◽  
Minmin Ma ◽  
Xinfeng Liu

Severe carotid stenosis or occlusion may cause insufficient blood flow and lead to distal artery wall collapse and extensive lumen contraction. Whether this ‘adaptive narrowing' can restitute after carotid recanalization is unclear. We report a patient with global ischemia due to occlusions of bilateral carotid and right vertebral arteries. The occluded left carotid was recanalized successfully with angioplasty and stenting. The adaptively narrowed distal carotid did not restitute immediately but regained its morphology 1 week after the procedure. Carotid adaptive narrow distal occlusion or stenosis may not regain its original morphology immediately but several days after recanalization. This knowledge is instructive for treating occlusive carotid diseases.


2015 ◽  
Vol 35 (9) ◽  
pp. 1928-1935 ◽  
Author(s):  
Lasse Bach Steffensen ◽  
Martin Bødtker Mortensen ◽  
Mads Kjolby ◽  
Mette Kallestrup Hagensen ◽  
Claus Oxvig ◽  
...  

Author(s):  
E Kouhi ◽  
Y S Morsi ◽  
S H Masood

A three-dimensional (3D) computational model of stenotic coronary artery bypass grafting (CABG) system with fluid—structure interaction (FSI) using realistic physiological conditions is introduced. Unsteady pulsatile blood flow is applied to the wall of non-linear deformable arteries over the systolic period. In the analysis, the arbitrarily Lagrangian—Eulerian (ALE) formulation is used to couple the fluid region and solid domain. The method couples the equations of the deformation of the artery wall and applies them as the fluid domain boundary condition. The flow distribution and haemodynamic forces are presented in terms of velocity profiles and temporal and spatial wall shear stresses (WSSs) at the distal area. Rapid changes in the flow fields are observed in the early stages of the cardiac cycle, which alters the location of the recirculation zone from the toe to the host bed and then to the heel. The migration of the recirculation zone, considering the effect of deformability of the artery wall, indicates the same trend as the rigid wall model according to the location of low and high WSSs. However, the WSSs in the critical areas such as toe, heel, and suture lines are found to have dramatic drops in magnitudes in comparison with those of the rigid wall model. This could initiate the promotion of intimal hyperplasia (IH) and may cause an early graft failure in CABG.


Author(s):  
Biyue Liu

Atherosclerosis is a disease of large- and medium-size arteries, which involves complex interactions between the artery wall and the blood flow. Both clinical observations and experimental results showed that the fluid shear stress acting on the artery wall plays a significant role in the physical processes which lead to atherosclerosis [1,2]. Therefore, a sound understanding of the effect of the wall shear stress on atherosclerosis is of practical importance to early detection, prevention and treatment of the disease. A considerable number of studies have been performed to investigate the flow phenomena in human carotid artery bifurcations or curved tubes during the past decades [3–8]. Numerical studies have supported the experimental results on the correlation between blood flow parameters and atherosclerosis [6–8]. The objective of this work is to understand the effect of the wall shear stress on atherosclerosis. The mathematical description of pulsatile blood flows is modeled by applying the time-dependent, incompressible Navier-Stokes equations for Newtonian fluids. The equations of motion and the incompressibility condition are ρut+ρ(u·∇)u=−∇p+μΔu,  inΩ,    (1)∇·u=0,  inΩ    (2) where ρ is the density of the fluid, μ is the viscosity of the fluid, u = (u1, u2, u3) is the flow velocity, p is the internal pressure, Ω is a curved tube with wall boundary Γ (see Figure 1). At the inflow boundary, fully developed velocity profiles corresponding to the common carotid velocity pulse waveform are prescribed u2=0,u3=0,u1=U(1+Asin(2πt/tp)),    (3) where A is the amplitude of oscillation, tp is the period of oscillation; U is a fully developed velocity profile at the symmetry entrance plane. At the outflow boundary, surface traction force is prescribed as Tijnjni=0,    (4)uiti=0    (5) where Tij=−pδij+μ(∂ui/∂xj+∂uj/∂xi)    (6) is the stress tensor, n = (n1, n2, n3) is the out normal vector of the outlet boundary. On the wall boundary Γ, we assume that no slipping takes place between the fluid and the wall, no penetration of the fluid through the artery wall occurs: u|r=nHt,    (7) where n = (n1, n2, n3) is the out normal vector of the wall boundary Γ. H is the function representing the location of the wall boundary. At initial time t = 0, H is input as shown in Figure 1. During the computation, H is updated by a geometry update condition based on the localized blood flow information. The initial condition is prescribed as u|t=0=u0,p|t=0=p0, where u0, p0 can be obtained by solving a Stokes problem: −μΔu0+∇p0=0,∇·u0=0, with boundary conditions (3)–(7) but zero in the right hand side of (7).


Author(s):  
Sang Hoon Lee ◽  
Hyoung Gwon Choi ◽  
Jung Yul Yoo

To investigate the effect of the flexible artery wall on the flow field and to determine the wall shear stresses in the carotid artery wall, numerical simulations for the blood flow are carried out. For solving the equation of motion for the structure in typical fluid-structure interaction (FSI) problems, it is necessary to calculate the fluid force on the surface of the structure explicitly. To avoid the complexity due to the necessity of additional mechanical constraints, we use the combined formulation which includes both the fluid and structure equations of motion into single coupled variational equation. The Navier-Stokes equations for fluid flow are solved using a P2P1 Galerkin finite element method (FEM) and mesh movement is achieved using arbitrary Lagrangian-Eulerian (ALE) formulation. The Newmark method is employed for solving the dynamic equilibrium equations for linear elastic solid mechanics. The time-dependent, three-dimensional, incompressible flows of Newtonian fluids constrained in the flexible wall are analyzed. The study shows strongly skewed axial velocity and flow separation in the internal carotid artery (ICA). Flow separation results in locally low wall shear stress. Further, strong secondary motion in the ICA is observed.


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