Spatial comparison between wall shear stress measures and porcine arterial endothelial permeability

2004 ◽  
Vol 286 (5) ◽  
pp. H1916-H1922 ◽  
Author(s):  
Heather A. Himburg ◽  
Deborah M. Grzybowski ◽  
Andrew L. Hazel ◽  
Jeffrey A. LaMack ◽  
Xue-Mei Li ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Evans Blue ◽  
Fluid Dynamic ◽  
Endothelial Permeability ◽  
Blue Dye ◽  
Evans Blue Dye ◽  
Wall Shear ◽  
And Function

A better understanding of how hemodynamic factors affect the integrity and function of the vascular endothelium is necessary to appreciate more fully how atherosclerosis is initiated and promoted. A novel technique is presented to assess the relation between fluid dynamic variables and the permeability of the endothelium to macromolecules. Fully anesthetized, domestic swine were intravenously injected with the albumin marker Evans blue dye, which was allowed to circulate for 90 min. After the animals were euthanized, silicone casts were made of the abdominal aorta and its iliac branches. Pulsatile flow calculations were subsequently made in computational regions derived from the casts. The distribution of the calculated time-dependent wall shear stress in the external iliac branches was directly compared on a point-by-point basis with the spatially varying in vivo uptake of Evans blue dye in the same arteries. The results indicate that in vivo endothelial permeability to albumin decreases with increasing time-average shear stress over the normal range. Additionally, endothelial permeability increases slightly with oscillatory shear index.

Inter-Operator Segmentation Differences Impact Wall Shear Stress Distributions in Patient-Specific Computational Fluid Dynamic Models

2009 ◽  
Author(s):  
Ian C. Campbell ◽  
William W. Sprague ◽  
Marina Piccinelli ◽  
Alessandro Veneziani ◽  
John N. Oshinski
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Dynamic Models ◽  
Fluid Dynamic ◽  
Cfd Modeling ◽  
Patient Specific ◽  
Wall Thickening ◽  
Cross Sectional ◽  
Wall Shear

The link between hemodynamic forces, notably wall shear stress (WSS), and atherogenesis is well established. Patient-specific computational fluid dynamics (CFD) modeling of human vasculature has attracted recent attention because it allows investigators to determine areas at risk for plaque formation and subsequent rupture [1]. Non-invasive in vivo imaging methods such as magnetic resonance (MR) angiography allow acquisition of vascular geometry and cross-sectional velocity such that a CFD model can determine the spatial distribution of WSS. WSS may then be correlated with phenomena such as wall thickening.

Redox Signaling in an In Vivo Murine Model of Tailored Wall Shear Stress

2009 ◽  
Author(s):  
Nick J. Willett ◽  
John Oshinski ◽  
Don Giddens ◽  
Robert Guldberg ◽  
W. Robert Taylor
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Protein Expression ◽  
Fluid Dynamic ◽  
Inflammatory Marker ◽  
Inflammatory Protein ◽  
Wall Shear ◽  
Acute Changes ◽  
High Degree

Wall Shear Stress (WSS) has been identified as an important factor in the pathogenesis of atherosclerosis. We developed a novel murine aortic coarctation model to alter the hemodynamic environment in vivo. The model utilizes the shape memory response of nitinol clips to provide a high degree of control over aortic diameter and subsequently WSS. We employed this model to test the hypothesis that acute changes in WSS in vivo induce upregulation of inflammatory proteins mediated by Reactive Oxygen Species (ROS). WSS was mapped through a computational fluid dynamic model and correlated to inflammatory marker expression. C57B16 control mice were compared to tempol treated, apocynin treated, p47phox KO, and catalase overexpressor mice in this study. The results show that the coarctation produces low mean oscillatory WSS in the region downstream of the clip. The WSS in this region correlates to a large increase in VCAM-1 expression in wild-type mice. This WSS dependent increase in protein expression is unchanged in animal models of decreased ROS. This suggests that although the redox state is important to the overall pathogenesis of the disease, individual ROS or ROS sources may not be sufficient to inhibit a WSS dependent inflammatory response. Further analysis with this model utilizing other reagent treatments, transgenic mice, and markers will allow us to analyze the functional contribution of transcription factors, ROS, and ROS sources to WSS dependent inflammatory protein expression.

scholarly journals An In Vivo Murine Model of Low-Magnitude Oscillatory Wall Shear Stress to Address the Molecular Mechanisms of Mechanotransduction—Brief Report

2010 ◽  
Vol 30 (11) ◽  
pp. 2099-2102 ◽  
Author(s):  
Nick J. Willett ◽  
Robert C. Long ◽  
Kathryn Maiellaro-Rafferty ◽  
Roy L. Sutliff ◽  
Richard Shafer ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Murine Model ◽  
Molecular Mechanisms ◽  
Wall Shear ◽  
Low Magnitude

In Vivo Association Between Low Wall Shear Stress and Plaque in Subjects With Asymmetrical Carotid Atherosclerosis

Stroke ◽  
1997 ◽  
Vol 28 (5) ◽  
pp. 993-998 ◽  
Author(s):  
Agostino Gnasso ◽  
Concetta Irace ◽  
Claudio Carallo ◽  
Maria Serena De Franceschi ◽  
Corradino Motti ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Carotid Atherosclerosis ◽  
Wall Shear

scholarly journals Selectin-mediated rolling of neutrophils on immobilized platelets

Blood ◽  
1993 ◽  
Vol 82 (4) ◽  
pp. 1165-1174 ◽  
Author(s):  
SM Buttrum ◽  
R Hatton ◽  
GB Nash
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Shape Change ◽  
Vascular Occlusion ◽  
Rolling Velocity ◽  
Cell Shape Change ◽  
Cell Velocity ◽  
The Mean ◽  
Wall Shear

Abstract Interaction between neutrophils and platelets at the site of vascular damage or in ischaemic tissue may promote thrombosis and/or vascular occlusion. To study this interaction, we have developed a novel technique that allows visualization of adhesion of flowing neutrophils to immobilized, activated platelets. The total number of adherent neutrophils decreased with increasing wall shear stress in the range 0.05 to 0.4 Pa. Although a proportion of the adherent neutrophils were stationary, most were rolling with a velocity greater than 0.4 micron/s. The percentage of rolling cells increased with increasing wall shear stress, but the mean rolling cell velocity was nearly independent of shear stress. Adhesion of neutrophils was nearly abolished by treatment of the platelets with antibody to P-selectin, or by treatment of neutrophils with either neuraminidase, dextran sulfate, or EDTA. Studies with a series of antibodies to L-selectin (TQ-1, Dreg- 56, LAM1–3, and LAM1–10) suggested that this molecule was one neutrophil ligand for rolling adhesion. Thus, sialylated carbohydrate on neutrophils appears essential for P-selectin-mediated adhesion, and a proportion of this ligand may be presented by L-selectin. Treatment of the neutrophils with N-formyl-methionyl-leucyl-phenylalanine decreased the number of rolling cells, and increased the rolling velocity, possibly due to shedding of neutrophil ligand(s) and/or cell shape change. In vivo, immobilized platelets could play an important role in promoting attachment of neutrophils to vessel walls, eg, by slowing neutrophils so that integrin-mediated immobilization could occur.

Exploring High Frequency Temporal Fluctuations in the Terminal Aneurysm of the Basilar Bifurcation

2012 ◽  
Vol 134 (9) ◽  
Author(s):  
Matthew D. Ford ◽  
Ugo Piomelli
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
High Frequency ◽  
Cerebral Aneurysms ◽  
Patient Specific ◽  
Disturbed Flow ◽  
Frequency Fluctuations ◽  
Wall Shear ◽  
Inflow Jet

Cerebral aneurysms are a common cause of death and disability. Of all the cardiovascular diseases, aneurysms are perhaps the most strongly linked with the local fluid mechanic environment. Aside from early in vivo clinical work that hinted at the possibility of high-frequency intra-aneurysmal velocity oscillations, flow in cerebral aneurysms is most often assumed to be laminar. This work investigates, through the use of numerical simulations, the potential for disturbed flow to exist in the terminal aneurysm of the basilar bifurcation. The nature of the disturbed flow is explored using a series of four idealized basilar tip models, and the results supported by four patient specific terminal basilar tip aneurysms. All four idealized models demonstrated instability in the inflow jet through high frequency fluctuations in the velocity and the pressure at approximately 120 Hz. The instability arises through a breakdown of the inflow jet, which begins to oscillate upon entering the aneurysm. The wall shear stress undergoes similar high-frequency oscillations in both magnitude and direction. The neck and dome regions of the aneurysm present 180 deg changes in the direction of the wall shear stress, due to the formation of small recirculation zones near the shear layer of the jet (at the frequency of the inflow jet oscillation) and the oscillation of the impingement zone on the dome of the aneurysm, respectively. Similar results were observed in the patient-specific models, which showed high frequency fluctuations at approximately 112 Hz in two of the four models and oscillations in the magnitude and direction of the wall shear stress. These results demonstrate that there is potential for disturbed laminar unsteady flow in the terminal aneurysm of the basilar bifurcation. The instabilities appear similar to the first instability mode of a free round jet.

Distribution of Mass Transfer Rate and Wall Shear Stress Behind Simple Rectangular Stenosis in Pulsating Flow

1989 ◽  
Vol 111 (1) ◽  
pp. 47-54 ◽  
Author(s):  
R. Yamaguchi
Keyword(s):  
Mass Transfer ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Transfer Rate ◽  
Schmidt Number ◽  
Fluid Dynamic ◽  
Mass Transfer Rate ◽  
Pulsating Flow ◽  
Flow Through ◽  
Wall Shear

The distributions of mass transfer rate and wall shear stress in sinusoidal laminar pulsating flow through a two-dimensional asymmetric stenosed channel have been studied experimentally and numerically. The distributions are measured by the electrochemical method. The measurement is conducted at a Reynolds number of about 150, a Schmidt number of about 1000, a nondimensional pulsating frequency of 3.40, and a nondimensional flow amplitude of 0.3. It is suggested that the deterioration of an arterial wall distal to stenosis may be greatly enhanced by fluid dynamic effects.

Design and Analysis of a Shear Stress Sensor for Microcirculation Investigations (Invited Paper)

2003 ◽  
Author(s):  
Risa Robinson ◽  
Lynn Fuller ◽  
Harvey Palmer ◽  
Mary Frame
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Computational Technique ◽  
Flow Modification ◽  
Stress Sensors ◽  
Shear Stress Sensors ◽  
Wall Shear

Blood flow regulation in the microvascular network has been investigated by means of computational fluid dynamics, in vivo particle tracking and microchannel models. It is evident from these studies that shear stress along the wall is a key factor in the communication network that results in blood flow modification, yet current methods for shear stress determination are acknowledged to be imprecise. Micromachining technology allows for the development of implantable shear stress sensors that will enable us to monitor wall shear stress at multiple locations in arteriole bifurcations. In this study, a microchannel was employed as an in vitro model of a microvessel. Thermal shear stress sensors were used to mimic the endothelial cells that line the vessel wall. A three dimensional computational model was created to simulate the system’s thermal response to the constant temperature control circuit and related wall shear stress. The model geometry included a silicon wafer section with all the fabrication layers — silicon dioxide, poly silicon resistor, silicon nitride — and a microchannel with cross section 17 μm × 17 μm. This computational technique was used to optimize the dimensions of the system for a 0.01 Reynolds number flow at room temperature in order to reduce the amount of heat lost to the substrate and to predict and maximize the signal response. Results of the design optimization are presented and the fabrication process discussed.

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