Importance of Axial Stress in Arterial Growth and Remodeling

Author(s):  
J. D. Humphrey

Since the mid-1970s, we have continued to understand better the fundamental importance of mechanotransduction in vascular biology. For example, beginning with Rosen and colleagues in 1974, we discovered that endothelial cells alter their production of vasoactive molecules in response to changes in flow-induced wall shear stress; beginning with Glagov and colleagues in 1976, we discovered that vascular smooth muscle cells alter their production of extracellular matrix proteins in response to changes in cyclic stretching comparable to that induced by pulsatile pressures [1]. Indeed, such findings are not surprising given the well know arterial adaptations that occur in response to sustained changes in blood flow or pressure. The caliber of an artery tends to increase (or decrease) in response to sustained increases (decreases) in blood flow and the thickness of the arterial wall tends to increase (or decrease) in response to sustained increases (decreases) in blood pressure. In both cases, it appears that the associated wall shear or intramural circumferential stresses are returned toward normal following the change in hemodynamics.

2020 ◽  
Vol 88 (2) ◽  
Author(s):  
Yuxi Jia ◽  
Kumaradevan Punithakumar ◽  
Michelle Noga ◽  
Arman Hemmati

Abstract The characteristics of blood flow in an abnormal pediatric aorta with an aortic coarctation and aortic arch narrowing are examined using direct numerical simulations and patient-specific boundary conditions. The blood flow simulations of a normal pediatric aorta are used for comparison to identify unique flow features resulting from the aorta geometrical anomalies. Despite flow similarities compared to the flow in normal aortic arch, the flow velocity decreases with an increase in pressure, wall shear stress, and vorticity around both anomalies. The presence of wall shear stresses in the trailing indentation region and aorta coarctation opposing the primary flow direction suggests that there exist recirculation zones in the aorta. The discrepancy in relative flowrates through the top and bottom of the aorta outlets, and the pressure drop across the coarctation, implies a high blood pressure in the upper body and a low blood pressure in the lower body. We propose using flow manipulators prior to the aortic arch and coarctation to lower the wall shear stress, while making the recirculation regions both smaller and weaker. The flow manipulators form a guide to divert and correct blood flow in critical regions of the aorta with anomalies.


2012 ◽  
Vol 12 (01) ◽  
pp. 1250006 ◽  
Author(s):  
MALIKEH NABAEI ◽  
NASSER FATOURAEE

The mechanics of cerebral aneurysm pathogenesis, evolution and rupture are not yet well understood. This paper presents a numerical analysis of the formation of a saccular cerebral aneurysm in for the first time in a 3D model of the basilar artery bifurcation under normal and hypertensive blood pressure. Due to the excessive endothelium derived nitric oxide produced in high wall shear stress, we assumed that smooth muscle cell relaxation is the origin of the aneurysm formation. Arterial wall remodeling under constant tension was considered to be the other mechanism of disease evolution. The wall was constructed from two elastic and hyperelastic isotropic regions. The flow was considered steady, laminar, Newtonian, and incompressible. The fully coupled fluid and structure models were solved with the finite elements package ADINA 8.5. The wall shear stress, effective stress and deformation distributions under normal and hypertensive blood pressure were compared to a healthy bifurcation. The model shows that although the malfunction of the endothelial cell layer and the corresponding smooth muscle cell-related loss of vascular tone is important to the inception of the disease; A saccular aneurysm may not be formed by this mechanism alone, and also requires the fiber-related arterial wall remodeling for further development.


2021 ◽  
Vol 12 ◽  
Author(s):  
Sandrine Morel ◽  
Sabine Schilling ◽  
Mannekomba R. Diagbouga ◽  
Matteo Delucchi ◽  
Marie-Luce Bochaton-Piallat ◽  
...  

Background: Intracranial aneurysms (IAs) result from abnormal enlargement of the arterial lumen. IAs are mostly quiescent and asymptomatic, but their rupture leads to severe brain damage or death. As the evolution of IAs is hard to predict and intricates medical decision, it is essential to improve our understanding of their pathophysiology. Wall shear stress (WSS) is proposed to influence IA growth and rupture. In this study, we investigated the effects of low and supra-high aneurysmal WSS on endothelial cells (ECs).Methods: Porcine arterial ECs were exposed for 48 h to defined levels of shear stress (2, 30, or 80 dyne/cm2) using an Ibidi flow apparatus. Immunostaining for CD31 or γ-cytoplasmic actin was performed to outline cell borders or to determine cell architecture. Geometry measurements (cell orientation, area, circularity and aspect ratio) were performed on confocal microscopy images. mRNA was extracted for RNAseq analysis.Results: ECs exposed to low or supra-high aneurysmal WSS were more circular and had a lower aspect ratio than cells exposed to physiological flow. Furthermore, they lost the alignment in the direction of flow observed under physiological conditions. The effects of low WSS on differential gene expression were stronger than those of supra-high WSS. Gene set enrichment analysis highlighted that extracellular matrix proteins, cytoskeletal proteins and more particularly the actin protein family were among the protein classes the most affected by shear stress. Interestingly, most genes showed an opposite regulation under both types of aneurysmal WSS. Immunostainings for γ-cytoplasmic actin suggested a different organization of this cytoskeletal protein between ECs exposed to physiological and both types of aneurysmal WSS.Conclusion: Under both aneurysmal low and supra-high WSS the typical arterial EC morphology molds to a more spherical shape. Whereas low WSS down-regulates the expression of cytoskeletal-related proteins and up-regulates extracellular matrix proteins, supra-high WSS induces opposite changes in gene expression of these protein classes. The differential regulation in EC gene expression observed under various WSS translate into a different organization of the ECs’ architecture. This adaptation of ECs to different aneurysmal WSS conditions may affect vascular remodeling in IAs.


2016 ◽  
Vol 08 (07) ◽  
pp. 1640011 ◽  
Author(s):  
Martin E. Goodman ◽  
X. Y. Luo ◽  
N. A. Hill

In this paper, we present a mathematical model linking blood flow, shear-dependent endothelium permeability and intimal thickening (hyperplasia) of the arterial wall, which is an initial stage in the development of atherosclerosis. The key concepts are that the intimal layer swells in response to the presence of excess oxidised LDL (OxLDL) in foam cells. The hyperplasia disturbs blood flow, affecting endothelial permeability via the wall shear stress (WSS). These changes produce a feedback mechanism. LDL is transported through the arterial wall by advection and diffusion, and the concentration of LDL at each time step is assumed to be quasi-steady since it equilibrates on a fast time scale. The process is controlled by the slow timescale of the increase in concentration of OxLDL. We consider a section of uniform axisymmetric artery, and impose an initial local injury or ‘hotspot’ of relatively high permeability that enhances the influx of LDL, triggering the development of a bump-shaped lesion. In the absence of further inflammatory processes, the lesion eventually decays back to the homeostatic state. The model is used to explore how the shape of the lesion changes over time, its effect on WSS, influx rates of LDL and the sensitivity of these processes to oxidation parameters. The lesion is shown to propagate downstream driven by regions of high and low WSS on either side of the bump, and it persists for some time after the hotspot has vanished, leaving ample time for further pro-atherogenic processes to develop.


2020 ◽  
Vol 59 (SK) ◽  
pp. SKKE16 ◽  
Author(s):  
Ryo Nagaoka ◽  
Kazuma Ishikawa ◽  
Michiya Mozumi ◽  
Magnus Cinthio ◽  
Hideyuki Hasegawa

Physiology ◽  
2009 ◽  
Vol 24 (1) ◽  
pp. 58-71 ◽  
Author(s):  
George Osol ◽  
Maurizio Mandala

Sufficient uteroplacental blood flow is essential for normal pregnancy outcome and is accomplished by the coordinated growth and remodeling of the entire uterine circulation, as well as the creation of a new fetal vascular organ: the placenta. The process of remodeling involves a number of cellular processes, including hyperplasia and hypertrophy, rearrangement of existing elements, and changes in extracellular matrix. In this review, we provide information on uterine blood flow increases during pregnancy, the influence of placentation type on the distribution of uterine vascular resistance, consideration of the patterns, nature, and extent of maternal uterine vascular remodeling during pregnancy, and what is known about the underlying cellular mechanisms.


2021 ◽  
Author(s):  
Chandan Kumawat ◽  
Bhupendra Kumar Sharma ◽  
Khalid Saad Mekheimer

Abstract A two-phase blood flow model is considered to analyze the fluid flow and heat transfer in a curved tube with time-variant stenosis. In both core and plasma regions, the variable viscosity model ( Hematocrit and non linear temperature-dependent, respectively) is considered. A toroidal coordinate system is considered to describe the governing equations. The perturbation technique in terms of perturbation parameter ε is used to obtain the temperature profile of blood flow. In order to find the velocity, wall shear stress and impedance profiles, a second-order finite difference method is employed with the accuracy of 10−6 in the each iteration. Under the conditions of fully-developed flow and mild stenosis, the significance of various physical parameters on the blood velocity, temperature, wall shear stress (WSS) and impedance are investigated with the help of graphs. A validation of our results has been presented and comparison has been made with the previously published work and present study, and it revels the good agreement with published work. The present mathematical study suggested that arterial curvature increase the fear of deposition of plaque (atherosclerosis), while, the use of thermal radiation in heat therapies lowers this risk. The positive add in the value of λ1 causes to increase in plasma viscosity; as a result, blood flow velocity in the stenosed artery decreases due to the assumption of temperature-dependent viscosity of the plasma region. Clinical researchers and biologists can adopt the present mathematical study to lower the risk of lipid deposition, predict cardiovascular disease risk and current state of disease by understanding the symptomatic spectrum, and then diagnose patients based on the risk.


Sign in / Sign up

Export Citation Format

Share Document