Hemodynamics of the Rat Aortic Arch

2012 ◽  
Author(s):  
David S. Molony ◽  
Andrew Nencka ◽  
Zhixin Li ◽  
Ming Zhao ◽  
Don P. Giddens
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vascular Disease ◽  
Molecular Level ◽  
In Vivo Studies ◽  
Mechanical Stimuli ◽  
Model Studies ◽  
Plaque Development ◽  
Wall Shear

Hemodynamics have been linked to the genesis and progress of vascular disease in humans and animals1. Disturbed flow patterns such as stagnant flow or flow reversal lead to low or oscillating wall shear stress (WSS). Several in-vivo studies have correlated these types of WSS with disease formation1, 2. The desire to find correlations between markers of vascular disease and mechanical stimuli and because of their easier availability has led to an increasing number of animal model studies. The mouse, in particular, is a commonly used animal for investigating vascular disease formation and progression. Suo et al., were one of the first to relate findings on the molecular level with WSS1. They found increased VCAM and ICAM expression in areas of low WSS. More recently Hoi et al.2, have shown a correlation between atherosclerotic plaque development and hemodynamic parameters such as low time averaged wall shear stress (TAWSS) and Oscillatory Shear Index (OSI).

Differential Gene Expression of Endothelial Cells Under High Wall Shear Stress and Spatial Gradients

2010 ◽  
Author(s):  
Jennifer Dolan ◽  
Song Liu ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Cerebral Aneurysms ◽  
In Vivo Studies ◽  
Spatial Gradient ◽  
Flow Acceleration ◽  
Spatial Gradients ◽  
Wall Shear

In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature. Due to the focal nature of aneurysm development it has long been speculated that hemodynamics are an important factor in aneurysm susceptibility. The local hemodynamics of bifurcations are complex, being characterized by flow impingement causing a high frictional force on the vessel wall known as wall shear stress (WSS) and significant flow acceleration or deceleration, manifested as the positive or negative spatial gradient of WSS (WSSG). In vivo studies have recently identified that aneurysm initiation occurs at areas of the vessel wall that experience a combination of both high WSS and positive WSSG [1,2]

Positive and Negative Wall Shear Stress Gradients Have Different Effects on Endothelial Phenotype Under High Wall Shear Stress

2011 ◽  
Author(s):  
Jennifer Dolan ◽  
Frasier Sim ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Cerebral Aneurysms ◽  
In Vivo Studies ◽  
Spatial Gradient ◽  
Cerebral Vasculature ◽  
High Wall Shear Stress ◽  
Wall Shear

In both human and animal models, cerebral aneurysms tend to develop at the apices of bifurcations in the cerebral vasculature where the blood vessel wall experiences complex hemodynamics. In vivo studies have recently revealed that the initiation of cerebral aneurysms is confined to a well-defined hemodynamic microenvironment [1,2]. Metaxa et al. [2] found that early aneurysm remodeling initiates where the vessel wall experiences high wall shear stress (WSS) and flow is accelerating, thus creating a positive spatial gradient in WSS (WSSG). Closer examination of such in vivo studies reveals that exposure of the vessel wall to equally high WSS in the presence of decelerating flow, that is, negative WSSG, does not result in aneurysm-like destruction.

Differential Responses of Endothelial Cells to Positive and Negative Wall Shear Stress Gradients

2010 ◽  
Author(s):  
Jennifer Dolan ◽  
Sukhjinder Singh ◽  
Hui Meng ◽  
John Kolega
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Vessel Wall ◽  
Fluid Shear Stress ◽  
Cerebral Aneurysms ◽  
In Vivo Studies ◽  
Outer Side ◽  
Fluid Shear ◽  
Wall Shear

Cerebral aneurysms tend to develop at bifurcation apices or the outer side of curved vessels where the blood vessel wall experiences complex hemodynamics. In vivo studies have recently revealed that the initiation of cerebral aneurysms is confined to a well-defined hemodynamic microenvironment. Specifically aneurysms form where the vessel wall experiences high fluid shear stress (wall shear stress, WSS) and flow is accelerating, so that the wall is exposed to a positive spatial gradient in the fluid shear stress (wall shear stress gradient, WSSG)[1,2]. Closer examination of such in vivo studies reveals that exposure of the vessel wall to equally high WSS in the presence of decelerating flow, that is, negative WSSG, does not result in aneurysm-like remodeling.

Numerical Simulation of Fluid-Induced Vibration and Wall Shear Stress in Fusi/Form Cerebral Aneurysm: Newtonian and Non-Newtonian Fluid

2006 ◽  
Author(s):  
Yong Hyun Kim ◽  
Joon Sand Lee ◽  
Xin Wu
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Newtonian Fluid ◽  
Stress Gradient ◽  
In Vivo Studies ◽  
Rupture Area ◽  
Study Results ◽  
Wall Shear

Vascular techniques have been used for curing the aneurysm, but the reason for the occurrence of aneurysms can not be known using these techniques. These techniques are usually used for preventing a significant situation such as rupture of an aneurysm. In our study, blood flow effects with or without vascular techniques inside an aneurysm were analyzed with computational fluid dynamics (CFD). Important hemodynamic quantities like wall shear stress and pressure in vessel are difficult to measure in-vivo. Blood flow is assumed to be Newtonian fluid. But it actually consists of platelets, so it is also considered a non-Newtonian fluid in this study. Results of the numerical model were used to compare and analyze fluid characteristics with experimental data. Using the flow characteristics (wall shear stress (WSS), wall shear stress gradient (WSSG)), the rupture area was identified to be located in the distal area. However, the rupture area, in vivo studies, was observed to be present at a different location. During pulsatile flow, vibration induced by flow is implicated by weakening of the artery wall and affects more than shear stress. After adapting the fluid-induced vibration, the rupture area in aneurysm is found to be located in the same area as the in-vivo result. Since smaller inflow and low WSS provide the effect of the distal neck, the vibration provides more effects in dome area. In this study it has been found that the effect of shear stress on the rupture of aneurysm is less than the effect of vibration. In the case of non-Newtonian fluid, vibration induced by flow also has more effects than WSS and WSSG. The simulation results gave detailed information about hemodynamics under physiological pulsatile inlet condition.

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.

The Effect of Wall Distensibility on Flow in a Two-Dimensional End-to-Side Anastomosis

1994 ◽  
Vol 116 (3) ◽  
pp. 294-301 ◽  
Author(s):  
D. A. Steinman ◽  
C. Ross Ethier
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Intimal Hyperplasia ◽  
Bypass Graft ◽  
Numerical Approach ◽  
Flow Patterns ◽  
Temporal Variations ◽  
Model Studies ◽  
Wall Shear ◽  
Wall Distensibility

The development of intimal hyperplasia at the distal anastomosis is the major cause of long-term bypass graft failure. To evaluate the suspected role of hemodynamic factors in the pathogenesis of distal intimal hyperplasia, an understanding of anastomotic flow patterns is essential. Due to the complexity of arterial flow, model studies typically make simplifying assumptions, such as treating the artery and graft walls as rigid. In the present study this restriction is relaxed to consider the effects of vessel wall distensibility on anastomotic flow patterns. Flow was simulated in an idealized 2-D distensible end-to-side anastomosis model, using parameters appropriate for the distal circulation and assuming a purely elastic artery wall. A novel numerical approach was developed in which the wall velocities are solved simultaneously with the fluid and pressure fields, while the wall displacements are treated via an iterative update. Both the rigid and distensible cases indicated the presence of elevated temporal variations and low average magnitudes of wall shear stress at sites known to be susceptible to the development of intimal hyperplasia. At these same sites, large spatial gradients of wall shear stress were also noted. Comparison between distensible-walled and corresponding rigid-walled simulations showed moderate changes in wall shear stress at isolated locations, primarily the bed, toe and heel. For example, in the case of a distensible geometry and a physiologic pressure waveform, the heel experienced a 38 percent increase in cycle-averaged shear stress, with a corresponding 15 percent reduction in shear stress variability, both relative to the corresponding values in the rigid-walled case. However, other than at these isolated locations, only minor changes in overall wall shear stress patterns were observed. While the physiological implications of such changes in wall shear stress are not known, it is suspected that the effects of wall distensibility are less pronounced than those brought about by changes in arterial geometry and flow conditions.

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.

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