Scaling laws for wall shear stress through stenoses under steady and pulsatile flow conditions

Author(s):  
LP Chua ◽  
S C M Yu ◽  
Q Xue
2014 ◽  
Vol 36 (10) ◽  
pp. 1233-1245 ◽  
Author(s):  
Foad Kabinejadian ◽  
Dhanjoo N. Ghista ◽  
Boyang Su ◽  
Mercedeh Kaabi Nezhadian ◽  
Leok Poh Chua ◽  
...  

1984 ◽  
Vol 106 (3) ◽  
pp. 552-557 ◽  
Author(s):  
K. V. Rao ◽  
B. F. Armaly ◽  
T. S. Chen

Laminar mixed forced and free convection from a line thermal source imbedded at the leading edge of an adiabatic vertical surface is analytically investigated for the cases of buoyancy assisting and buoyancy opposing flow conditions. Temperature and velocity distributions in the boundary layer adjacent to the adiabatic surface are presented for the entire range of the buoyancy parameter ξ (x) = Grx/Rex5/2 from the pure forced (ξ(x) = 0) to the pure free (ξ(x) = ∞) convection regime for fluids having Prandtl numbers of 0.7 and 7.0. For buoyancy-assisting flow, the velocity overshoot, the temperature, and the wall shear stress increase as the plume’s strength increases. On the other hand, the velocity overshoot, the wall shear stress, and the temperature decrease as the free-stream velocity increases. For buoyancy opposing flow, the velocity and wall shear stress decrease but the temperature increases as the plume’s strength increases.


2020 ◽  
Vol 61 (2) ◽  
Author(s):  
Andreas Bauer ◽  
Maximilian Bopp ◽  
Suad Jakirlic ◽  
Cameron Tropea ◽  
Axel Joachim Krafft ◽  
...  

2005 ◽  
Vol 128 (3) ◽  
pp. 347-359 ◽  
Author(s):  
Divakar Rajamohan ◽  
Rupak K. Banerjee ◽  
Lloyd H. Back ◽  
Ashraf A. Ibrahim ◽  
Milind A. Jog

A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530dyn∕cm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10dyn∕cm2 and a negative wall shear stress of −10dyn∕cm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.


1993 ◽  
Vol 265 (2) ◽  
pp. H553-H561 ◽  
Author(s):  
C. Alonso ◽  
A. R. Pries ◽  
P. Gaehtgens

The time-dependent flow behavior of normal human blood after a sudden reduction of wall shear stress from 5,000 mPa to a low level (2-100 mPa) was studied during perfusion of vertical tubes (internal diam 28-101 microns) at constant driving pressures. Immediately after the implementation of low-shear flow conditions the concentration of red blood cells (RBCs) near the tube wall started to decrease, and marginal plasma spaces developed as a result of the assembly of RBC aggregates. This was associated with a time-dependent increase of flow velocity by up to 200% within 300 s, reflecting a reduction of apparent viscosity. These time-dependent changes of flow behavior increased strongly with decreasing wall shear stress and with increasing tube diameter. A correlation between the width of the marginal plasma layer and relative apparent viscosity was obtained for every condition of tube diameter, wall shear stress, and time. Time-dependent changes of blood rheological properties could be relevant in the circulation, where the blood is exposed to rapid and repeated transitions from high-shear flow conditions in the arterial and capillary system to low-shear conditions in the venous system.


2012 ◽  
Vol 302 (8) ◽  
pp. C1109-C1118 ◽  
Author(s):  
Jennifer M. Dolan ◽  
Fraser J. Sim ◽  
Hui Meng ◽  
John Kolega

Chronic high flow can induce arterial remodeling, and this effect is mediated by endothelial cells (ECs) responding to wall shear stress (WSS). To assess how WSS above physiological normal levels affects ECs, we used DNA microarrays to profile EC gene expression under various flow conditions. Cultured bovine aortic ECs were exposed to no-flow (0 Pa), normal WSS (2 Pa), and very high WSS (10 Pa) for 24 h. Very high WSS induced a distinct expression profile compared with both no-flow and normal WSS. Gene ontology and biological pathway analysis revealed that high WSS modulated gene expression in ways that promote an anti-coagulant, anti-inflammatory, proliferative, and promatrix remodeling phenotype. A subset of characteristic genes was validated using quantitative polymerase chain reaction: very high WSS upregulated ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motif-1), PLAU (urokinase plasminogen activator), PLAT (tissue plasminogen activator), and TIMP3, all of which are involved in extracellular matrix processing, with PLAT and PLAU also contributing to fibrinolysis. Downregulated genes included CXCL5 and IL-8 and the adhesive glycoprotein THBS1 (thrombospondin-1). Expressions of ADAMTS1 and uPA proteins were assessed by immunhistochemistry in rabbit basilar arteries experiencing increased flow after bilateral carotid artery ligation. Both proteins were significantly increased when WSS was elevated compared with sham control animals. Our results indicate that very high WSS elicits a unique transcriptional profile in ECs that favors particular cell functions and pathways that are important in vessel homeostasis under increased flow. In addition, we identify specific molecular targets that are likely to contribute to adaptive remodeling under elevated flow conditions.


2003 ◽  
Vol 125 (2) ◽  
pp. 207-217 ◽  
Author(s):  
E. A. Finol ◽  
K. Keyhani ◽  
C. H. Amon

In the abdominal segment of the human aorta under a patient’s average resting conditions, pulsatile blood flow exhibits complex laminar patterns with secondary flows induced by adjacent branches and irregular vessel geometries. The flow dynamics becomes more complex when there is a pathological condition that causes changes in the normal structural composition of the vessel wall, for example, in the presence of an aneurysm. This work examines the hemodynamics of pulsatile blood flow in hypothetical three-dimensional models of abdominal aortic aneurysms (AAAs). Numerical predictions of blood flow patterns and hemodynamic stresses in AAAs are performed in single-aneurysm, asymmetric, rigid wall models using the finite element method. We characterize pulsatile flow dynamics in AAAs for average resting conditions by means of identifying regions of disturbed flow and quantifying the disturbance by evaluating flow-induced stresses at the aneurysm wall, specifically wall pressure and wall shear stress. Physiologically realistic abdominal aortic blood flow is simulated under pulsatile conditions for the range of time-average Reynolds numbers 50⩽Rem⩽300, corresponding to a range of peak Reynolds numbers 262.5⩽Repeak⩽1575. The vortex dynamics induced by pulsatile flow in AAAs is depicted by a sequence of four different flow phases in one period of the cardiac pulse. Peak wall shear stress and peak wall pressure are reported as a function of the time-average Reynolds number and aneurysm asymmetry. The effect of asymmetry in hypothetically shaped AAAs is to increase the maximum wall shear stress at peak flow and to induce the appearance of secondary flows in late diastole.


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