scholarly journals The influence of oxygen tension on the local regulation of blood flow by shear stress

2016 ◽  
Vol 15 (2) ◽  
pp. 60-64
Author(s):  
N. Kh. Shadrina
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Mathematical Simulation ◽  
Oxygen Tension ◽  
Flow Rate ◽  
Vessel Wall ◽  
Muscle Layer ◽  
No Production ◽  
Vessel Response

Introduction and purpose. Vascular response to mechanical stimuli, namely transmural pressure (Bayliss effect) and wall shear stress (response to blood flow), play an important role in regulation of vascular tone. The purpose of the work was to study an influence of hypoxia on the vessel radius and blood flow control by response to shear stress. Methodology/approach. Mathematical simulation was used. The model is based on published data of experiments on small cerebral arteries of rats. The main assumptions of the model are: 1) the vessel is a thin wall cylinder; 2) the radius is controlled by two parameters: concentration of free calcium ions in the cytoplasm of the smooth muscle cells and concentration of nitric oxide (NO) in the smooth muscle layer; 3) the rate of NO production by endothelium is proportional to modulus of shear stress on the vessel wall. The apparent blood viscosity is calculated using the solution of the problem of two-layer flow. The numerical experiments were performed in Turbo Pascal. The main results and discussion. The dependence of vessel tone regulation by response to altered shear stress on oxygen tension is caused by dependence of NO synthesis in endothelium and NO consumption on oxygen concentration. As it follows from mathematical simulation, hypoxia reduces the role of mechanogenic regulation, and the increase of the wall sensitivity to NO makes this effect more appreciable. Calculations performed for typical value of cerebral vessel response to shear stress, show that the fall in oxygen tension from 100 to 30 per cent leads to decrease in diameter by 6 %, in blood flow rate by 11 %. The rheological factors prevent flow rate diminution, but their contribution is very small: less than 3 %. The fall in oxygen tension reduces NO production rate by endothelial cells and NO concentration in the vessel wall. At strong hypoxia (reduction in oxygen tension from 100 to 30 % and less) NO concentration in smooth muscle layer drops by more than 15 %. Conclusions. Hypoxia decreases NO-dependent vessel response to altered shear rate. This effect increases with the value of vessel response to shear stress. The rheological factors impede the decrease of this response.

scholarly journals Shear stress and aneurysms: a review

2019 ◽  
Vol 47 (1) ◽  
pp. E2 ◽  
Author(s):  
Brittany Staarmann ◽  
Matthew Smith ◽  
Charles J. Prestigiacomo
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Wall Shear Stress ◽  
Smooth Muscle Cells ◽  
Frictional Force ◽  
Vessel Wall ◽  
Risk Of Rupture ◽  
Aneurysm Growth

Wall shear stress, the frictional force of blood flow tangential to an artery lumen, has been demonstrated in multiple studies to influence aneurysm formation and risk of rupture. In this article, the authors review the ways in which shear stress may influence aneurysm growth and rupture through changes in the vessel wall endothelial cells, smooth-muscle cells, and surrounding adventitia, and they discuss shear stress–induced pathways through which these changes occur.

Shear stress inhibits smooth muscle cell migration via nitric oxide-mediated downregulation of matrix metalloproteinase-2 activity

2005 ◽  
Vol 288 (5) ◽  
pp. H2244-H2252 ◽  
Author(s):  
Jeffrey S. Garanich ◽  
Manolis Pahakis ◽  
John M. Tarbell
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Matrix Metalloproteinase ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Matrix Metalloproteinase 2 ◽  
No Production ◽  
No Donor ◽  
Western Blots

Vascular smooth muscle cell (SMC) migration is a hallmark of intimal hyperplasia (IH), the progression of which is affected by hemodynamic conditions at the diseased site. The realization that SMCs are exposed to blood flow in both denuded vessels (direct blood flow) and intact vessels (interstitial blood flow) motivated this study of the effects of fluid flow shear stress (SS) on SMC migration. Rat aortic SMCs were seeded onto Matrigel-coated cell culture inserts, and their migratory activity toward PDGF-BB when exposed to SS in a rotating disk apparatus was quantified. Four hours of either 10 or 20 dyn/cm2 SS significantly inhibited SMC migration to the bottom side of the insert. This inhibition was associated with downregulation of SMC matrix metalloproteinase (MMP)-2 activation. Four hours of 10 dyn/cm2 SS also drastically increased SMC production of NO. A NO synthase inhibitor ( NG-nitro-l-arginine methyl ester; 100 μM) abolished the shear-induced increase in SMC NO production as well as the inhibition of migration and MMP-2 activity. A NO donor ( S-nitroso- N-acetyl-penicillamine; 500 μM) suppressed SMC migration via the reduction of both total and active MMP-2 levels. Addition of 10 μM MMP-2 inhibitor I to inserts significantly reduced SMC migration. Western blots showed no effect of 4 h of 20 dyn/cm2 SS on SMC production of PDGF-AA, another chemical known to suppress SMC migration. Thus it appears that SS acts to suppress SMC migration by upregulating the cellular production of NO, which in turn inhibits MMP-2 activity.

scholarly journals Autoregulation and mechanotransduction control the arteriolar response to small changes in hematocrit

2012 ◽  
Vol 303 (9) ◽  
pp. H1096-H1106 ◽  
Author(s):  
Krishna Sriram ◽  
Beatriz Y. Salazar Vázquez ◽  
Amy G. Tsai ◽  
Pedro Cabrales ◽  
Marcos Intaglietta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Shear Stress ◽  
Carrying Capacity ◽  
Vessel Wall ◽  
Solid Mechanics ◽  
No Production ◽  
Myogenic Response ◽  
Analytic Model ◽  
Beneficial Effects

Here, we present an analytic model of arteriolar mechanics that accounts for key autoregulation mechanisms, including the myogenic response and the vasodilatory effects of nitric oxide (NO) in the vasculature. It couples the fluid mechanics of blood flow in arterioles with solid mechanics of the vessel wall and includes the effects of wall shear stress- and stretch-induced endothelial NO production. The model can be used to describe the regulation of blood flow and NO transport under small changes in hematocrit and to analyze the regulatory response of arterioles to small changes in hematocrit. Our analysis revealed that the experimentally observed paradoxical increase in cardiac output with small increases in hematocrit results from the combination of increased NO production and the effects of a strong myogenic response modulated by elevated levels of WSS. Our findings support the hypothesis that vascular resistance varies inversely with blood viscosity for small changes in hematocrit in a healthy circulation that responds to shear stress stimuli. They also suggest beneficial effects independent of changes in O2carrying capacity associated with the postsurgical transfusion of one or two units of blood.

A model of anemic tissue perfusion after blood transfusion shows critical role of endothelial response to shear stress stimuli

2021 ◽  
Author(s):  
Weiyu Li ◽  
Amy G. Tsai ◽  
Marcos Intaglietta ◽  
Daniel M. Tartakovsky
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Blood Transfusion ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Arterial Blood Flow ◽  
Microvascular Blood Flow ◽  
No Production ◽  
Arterial Blood ◽  
Transfusion Requirements

­­ ­Although some of the cardiovascular responses to changes in hematocrit (Hct) are not fully quantified experimentally, available information is sufficient to build a mathematical model of the consequences of treating anemia by introducing RBCs into the circulation via blood transfusion. We present such a model, which describes how the treatment of normovolemic anemia with blood transfusion impacts oxygen (O2) delivery (DO2, the product of blood O2 content and arterial blood flow) by the microcirculation. Our analysis accounts for the differential response of the endothelium to the wall shear stress (WSS) stimulus, changes in nitric oxide (NO) production due to modification of blood viscosity caused by alterations of both hematocrit (Hct) and cell free layer thickness, as well as for their combined effects on microvascular blood flow and DO2. Our model shows that transfusions of 1- and 2-unit of blood have a minimal effect on DO2 if the microcirculation is unresponsive to the WSS stimulus for NO production that causes vasodilatation increasing blood flow and DO2. Conversely, in a fully WSS responsive organism, blood transfusion significantly enhances blood flow and DO2, because increased viscosity stimulates endothelial NO production causing vasodilatation. This finding suggests that evaluation of a patients' pre-transfusion endothelial WSS responsiveness should be beneficial in determining the optimal transfusion requirements for treating anemic patients.

Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses

2000 ◽  
Vol 279 (1) ◽  
pp. H279-H284 ◽  
Author(s):  
Kim A. Dora ◽  
David N. Damon ◽  
Brian R. Duling
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Third Order ◽  
Vasomotor Responses ◽  
Vasodilatory Response ◽  
Flow Through ◽  
Stress Dependent ◽  
Dependent Mechanism

In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-μm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10−4 M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.

Is the Maturation of Arteriovenous Fistulas a Mechanical or Biological Problem?

2016 ◽  
Author(s):  
Daniel Jodko ◽  
Damian Obidowski ◽  
Piotr Reorowicz ◽  
Krzysztof Jozwik
Keyword(s):  
High Pressure ◽  
Blood Flow ◽  
Shear Stress ◽  
Flow Rate ◽  
Blood Flow Rate ◽  
Average Diameter ◽  
Patient Specific ◽  
Maturation Process ◽  
Arteriovenous Fistulas ◽  
Biological Problem

During the maturation the high pressure blood from the artery inflows directly to the vein, extends its diameter, and finally the blood flow rate in the vein is even 500-times greater than normal one. The changes of the wall shear stress (WSS) in the vein are thought to play a key role in the remodelling of its wall. However, this process is still not well understood. The aim of this paper is to show an innovative approach for modelling of the vein deformation during the maturation process of a-v fistulas. Dilation of the vein was modelled as two-step complex biomechanical process. The obtained results concerning final diameter of the vein are compared with average diameter obtained for large group of patients. Moreover, this study shows the changes in the flow rate and the WSS that occur after maturation in the patient-specific fistula.

Erythropoietin Signaling and Response in Vascular Smooth Muscle Cells.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3724-3724
Author(s):  
Bojana B. Beleslin-Cokic ◽  
Vladan P. Cokic ◽  
Ljiljana Gojkovic-Bukarica ◽  
Constance Tom Noguchi
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Blood Vessel ◽  
Vascular Smooth Muscle ◽  
Oxygen Tension ◽  
Erythropoietin Receptor ◽  
No Production ◽  
Low Oxygen ◽  
Erythroid Progenitor ◽  
Low Oxygen Tension

Abstract Erythopoietin (EPO) and erythropoietin receptor (EPOR) regulate survival, proliferation, differentiation and viability of erythroid progenitor cells. Beyond erythropoiesis, we have observed that human vascular endothelial cells respond to EPO stimulation by inducing EPOR and endothelial nitric oxide synthase (eNOS) expression, increasing NO production and cGMP, particularly under low oxygen tension. In this study, we investigate the response of vascular smooth muscle (VSM) to EPO stimulation and the contribution of blood vessel to relaxation/contraction. We found that VSM cells express EPOR and that treatment with EPO (5 U/ml) at reduced oxygen tension increased EPOR mRNA by 2 fold. This increased EPO responsiveness at low oxygen tension is accompanied by increased cell proliferation at 2% O2 more than 2 fold. Unlike endothelial cells, EPO did not induce eNOS or NO production in VSM cells. PI-3 kinase was involved in EPO stimulation with no change in MAP kinase. In an isolated blood vessel model system, we checked EPO responsiveness. EPO produced contractions (0.32 ± 0.3 g) of rat renal artery, and pretreatment with LY294002 (10 mM), an inhibitor of PI-3 kinase, statistically significantly inhibited this contraction (58.7 ± 7%). This response was also observed with the endothelium layer removed. In preparations of human internal mammary artery (HIMA) and human saphenous vein (HSV) from patients undergoing coronary artery bypass, EPO did not affect basal vascular tone of HIMA and HSV with the endothelium layer removed, but EPO (5 U/ml) potentated noradrenalin-induced contraction by up to 2 fold in HSV and HIMA. Also, pretreatment with EPO significantly increase angiotensin-evoked contractions of these blood vessels (50 ± 8%, 113 ± 17%, respectively P < 0.01), suggesting that EPO has synergistic effects on angiotensin or noradrenalin-induced [Ca2+] mobilization, particularly on intracellular Ca2+ release. These data suggest that EPO stimulation of vascular smooth muscle may act to modulate or balance the vasodilatory effects of increased NO production by EPO stimulated endothelium. Under oxygen stress vascular smooth muscle can respond to EPO by proliferation and PI-3 kinase activation as a protective effect and in conjunction with Ca2+ release likely contributes to the overall vascular response.

Expression of VEGF and its receptors Flt-1 and Flk-1/KDR is altered in lambs with increased pulmonary blood flow and pulmonary hypertension

2003 ◽  
Vol 285 (1) ◽  
pp. L222-L231 ◽  
Author(s):  
Eugenia Mata-Greenwood ◽  
Barbara Meyrick ◽  
Scott J. Soifer ◽  
Jeffrey R. Fineman ◽  
Stephen M. Black
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Immunohistochemical Analysis ◽  
Muscle Layer ◽  
Pulmonary Epithelium ◽  
Pulmonary Vessel ◽  
Smooth Muscle Layer ◽  
Vegf Signaling

Utilizing in utero aortopulmonary vascular graft placement, we developed a lamb model of congenital heart disease and increased pulmonary blood flow. We showed previously that these lambs have increased pulmonary vessel number at 4 wk of age. To determine whether this was associated with alterations in VEGF signaling, we investigated vascular changes in expression of VEGF and its receptors, Flt-1 and KDR/Flk-1, in the lungs of shunted and age-matched control lambs during the first 8 wk of life. Western blot analysis demonstrated that VEGF, Flt-1, and KDR/Flk-1 expression was higher in shunted lambs. VEGF and Flt-1 expression was increased at 4 and 8 wk of age ( P <0.05). However, KDR/Flk-1 expression was higher in shunted lambs only at 1 and 4 wk of age ( P <0.05). Immunohistochemical analysis demonstrated that, in control and shunted lambs, VEGF localized to the smooth muscle layer of vessels and airways and to the pulmonary epithelium while increased VEGF expression was localized to the smooth muscle layer of thickened media in remodeled vessels in shunted lambs. VEGF receptors were localized exclusively in the endothelium of pulmonary vessels. Flt-1 was increased in the endothelium of small pulmonary arteries in shunted animals at 4 and 8 wk of age, whereas KDR/Flk-1 was increased in small pulmonary arteries at 1 and 4 wk of age. Our data suggest that increased pulmonary blood flow upregulates expression of VEGF and its receptors, and this may be important in development of the vascular remodeling in shunted lambs.

A Numerical Multiscale Study of the Haemodynamics in an Image-Based Model of Human Carotid Artery Bifurcation

2009 ◽  
Author(s):  
Diego Gallo ◽  
Raffaele Ponzini ◽  
Filippo Consolo ◽  
Diana Massai ◽  
Luca Antiga ◽  
...  
Keyword(s):  
Fluid Dynamics ◽  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Cardiovascular System ◽  
Vessel Wall ◽  
3D Model ◽  
Carotid Bifurcation ◽  
Wall Shear ◽  
Flow Division

The initiation and progression of vessel wall pathologies have been linked to disturbances of blood flow and altered wall shear stress. The development of computational techniques in fluid dynamics, together with the increasing performances of hardware and software allow to routinely solve problems on a virtual environment, helping to understand the role of biomechanics factors in the healthy and diseased cardiovascular system and to reveal the interplay of biology and local fluid dynamics nearly intractable in the past, opening to detailed investigation of parameters affecting disease progression. One of the major difficulties encountered when wishing to model accurately the cardiovascular system is that the flow dynamics of the blood in a specific vascular district is strictly related to the global systemic dynamics. The multiscale modelling approach for the description of blood flow into vessels consists in coupling a detailed model of the district of interest in the framework of a synthetic description of the surrounding areas of the vascular net [1]. In the present work, we aim at evaluating the effect of boundary conditions on wall shear stress (WSS) related vessel wall indexes and on bulk flow topology inside a carotid bifurcation. To do it, we coupled an image-based 3D model of carotid bifurcation (local computational domain), with a lumped parameters (0D) model (global domain) which allows for physiological mimicking of the haemodynamics at the boundaries of the 3D carotid bifurcation model here investigated. Two WSS based blood-vessel wall interaction descriptors, the Time Averaged WSS (TAWSS), and the Oscillating Shear Index (OSI) were considered. A specific Lagrangian-based “bulk” blood flow descriptor, the Helical Flow Index (HFI) [2], was calculated in order to get a “measure” of the helical structure in the blood flow. In a first analysis the effects of the coupled 0D models on the 3D model are evaluated. The results obtained from the multiscale simulation are compared with the results of simulations performed using the same 3D model, but imposing a flow rate at internal carotid (ICA) outlet section equal to the maximum (60%) and the minimum (50%) flow division obtained out from ICA in the multiscale model simulation (the presence of the coupled 0D model gives variable internal/external flow division ratio during the cardiac cycle), and a stress free condition on the external carotid (ECA).

Vascular smooth muscle cell glycocalyx modulates shear-induced proliferation, migration, and NO production responses

2011 ◽  
Vol 300 (1) ◽  
pp. H76-H83 ◽  
Author(s):  
Hongyan Kang ◽  
Yubo Fan ◽  
Xiaoyan Deng
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Heparan Sulfate ◽  
Muscle Cells ◽  
Flow Chamber ◽  
No Production ◽  
Physiological Level

The endothelial cell glycocalyx, a structure coating the luminal surface of the vascular endothelium, and its related mechanotransduction have been studied by many over the last decade. However, the role of vascular smooth muscle cells (SMCs) glycocalyx in cell mechanotransduction has triggered little attention. This study addressed the role of heparan sulfate proteoglycans (HSPGs), a major component of the glycocalyx, in the shear-induced proliferation, migration, and nitric oxide (NO) production of the rat aortic smooth muscle cells (RASMCs). A parallel plate flow chamber and a peristaltic pump were employed to expose RASMC monolayers to a physiological level of shear stress (12 dyn/cm2). Heparinase III (Hep.III) was applied to selectively degrade heparan sulfate on the SMC surface. Cell proliferation, migration, and NO production rates were determined and compared among the following four groups of cells: 1) untreated with no flow, 2) Hep.III treatment with no flow, 3) untreated with flow of 12 dyn/cm2 exposure, and 4) Hep.III treatment with flow of 12 dyn/cm2 exposure. It was observed that flow-induced shear stress significantly suppressed SMC proliferation and migration, whereas cells preferred to aligning along the direction of flow and NO production were enhanced substantially. However, those responses were not found in the cells with Hep.III treatment. Under flow condition, the heparinase III-treated cells remained randomly oriented and proliferated as if there were no flow presence. Disruption of HSPG also enhanced wound closure and inhibited shear-induced NO production significantly. This study suggests that HSPG may play a pivotal role in mechanotransduction of SMCs.

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