Experimental study of flow fields in an airway closure model

2010 ◽  
Vol 647 ◽  
pp. 391-402 ◽  
Author(s):  
S. BIAN ◽  
C.-F. TAI ◽  
D. HALPERN ◽  
Y. ZHENG ◽  
J. B. GROTBERG

The liquid lining in small human airways can become unstable and form liquid plugs that close off the airways. Bench-top experiments have been performed in a glass capillary tube as a model airway to study the airway instability and the flow-induced stresses on the airway walls. A microscale particle image velocimetry system is used to visualize quantitatively the flow fields during the dynamic process of airway closure. An annular film is formed by injecting low-viscosity Si-oil into the glycerol-filled capillary tube. The viscosity ratio between these two fluids is similar to that between water and air. The thickness of the film varies with the infusion rate of the core fluid, which is controlled by a syringe pump. After a uniform film is formed, the syringe pump is shut off so that the core flow speed is close to zero during closure. Instantaneous velocity fields in the annular film at various stages of airway closure are computed from the images and analysed. The wall shear stress at the instant when a liquid plug forms is found to be approximately one order of magnitude higher than the exponential growth period before closure. Within the short time span of the closure process, there are large wall shear stress fluctuations. Furthermore, dramatic velocity changes in the film flow during closure indicate a steep normal stress gradient on the airway wall. The experimental results show that the wall shear stress during closure can be high enough to injure airway epithelial cells. An airway that experiences closure and reopening cyclically during breathing could be injured from fluid forces during both phases of the cycle (i.e. inspiration and expiration).

2011 ◽  
Vol 677 ◽  
pp. 483-502 ◽  
Author(s):  
C.-F. TAI ◽  
S. BIAN ◽  
D. HALPERN ◽  
Y. ZHENG ◽  
M. FILOCHE ◽  
...  

The liquid lining in small human airways can become unstable and form liquid plugs that close off the airways. Direct numerical simulations are carried out on an airway model to study this airway instability and the flow-induced stresses on the airway walls. The equations governing the fluid motion and the interfacial boundary conditions are solved using the finite-volume method coupled with the sharp interface method for the free surface. The dynamics of the closure process is simulated for a viscous Newtonian film with constant surface tension and a passive core gas phase. In addition, a special case is examined that considers the core dynamics so that comparisons can be made with the experiments of Bian et al. (J. Fluid Mech., vol. 647, 2010, p. 391). The computed flow fields and stress distributions are consistent with the experimental findings. Within the short time span of the closure process, there are large fluctuations in the wall shear stress. Furthermore, dramatic velocity changes in the film during closure indicate a steep normal stress gradient on the airway wall. The computational results show that the wall shear stress, normal stress and their gradients during closure can be high enough to injure airway epithelial cells.


2011 ◽  
Vol 705 ◽  
pp. 258-279 ◽  
Author(s):  
Parsa Zamankhan ◽  
Brian T. Helenbrook ◽  
Shuichi Takayama ◽  
James B. Grotberg

AbstractWe study numerically the steady creeping motion of Bingham liquid plugs in two-dimensional channels as a model of mucus behaviour during airway reopening in pulmonary airways. In addition to flow analysis related to propagation of the plug, the stress distribution on the wall is studied for better understanding of potential airway epithelial cell injury mechanisms. The yield stress behaviour of the fluid was implemented through a regularized constitutive equation. The capillary number, $\mathit{Ca}$, and the Bingham number, $\mathit{Bn}$, which is the ratio of the yield stress to a characteristic viscous stress, varied over the ranges 0.025–0.1 and 0–1.5, respectively. For the range of parameters studied, it was found that, while the yield stress reduces the magnitude of the shearing along the wall, it can magnify the amplitude of the wall shear stress gradient significantly, and also it can elevate the magnitude of the wall shear stress and wall pressure gradient up to 30 % and 15 %, respectively. Therefore, the motion of mucus plugs can be more damaging to the airway epithelial cells due to the yield stress properties of mucus. The yield stress also modifies the profile of the plug where the amplitude of the capillary waves at the leading meniscus decreases with increase in $\mathit{Bn}$. Other findings are that: the thickness of the static film increases with increasing $\mathit{Bn}$; the driving pressure difference increases linearly with $\mathit{Bn}$; and increasing $\mathit{Bn}$ extends any wall stagnation point beneath the leading meniscus to an unyielded line segment beneath the leading meniscus. With an increase in $\mathit{Bn}$, the unyielded areas appear and grow in the adjacent wall film as well as the core region of the plug between the two menisci. The plug length, ${L}_{P} $, mostly modifies the topology of the yield surfaces. It was found that the unyielded area in the core region between the two menisci grows as the plug length decreases. The very short Bingham plug behaves like a solid lamella. In all computed liquid plugs moving steadily, the von Mises stress attains its maximum value near the interface of the leading meniscus in the transition region. For Bingham plugs moving very slowly, $\mathit{Ca}\ensuremath{\rightarrow} 0$, the driving pressure is non-zero.


2019 ◽  
Vol 131 (2) ◽  
pp. 442-452 ◽  
Author(s):  
Alexandra Lauric ◽  
James E. Hippelheuser ◽  
Adel M. Malek

OBJECTIVEEndothelium adapts to wall shear stress (WSS) and is functionally sensitive to positive (aneurysmogenic) and negative (protective) spatial WSS gradients (WSSG) in regions of accelerating and decelerating flow, respectively. Positive WSSG causes endothelial migration, apoptosis, and aneurysmal extracellular remodeling. Given the association of wide branching angles with aneurysm presence, the authors evaluated the effect of bifurcation geometry on local apical hemodynamics.METHODSComputational fluid dynamics simulations were performed on parametric bifurcation models with increasing angles having: 1) symmetrical geometry (bifurcation angle 60°–180°), 2) asymmetrical geometry (daughter angles 30°/60° and 30°/90°), and 3) curved parent vessel (bifurcation angles 60°–120°), all at baseline and double flow rate. Time-dependent and time-averaged apical WSS and WSSG were analyzed. Results were validated on patient-derived models.RESULTSNarrow symmetrical bifurcations are characterized by protective negative apical WSSG, with a switch to aneurysmogenic WSSG occurring at angles ≥ 85°. Asymmetrical bifurcations develop positive WSSG on the more obtuse daughter branch. A curved parent vessel leads to positive apical WSSG on the side corresponding to the outer curve. All simulations revealed wider apical area coverage by higher WSS and positive WSSG magnitudes, with increased bifurcation angle and higher flow rate. Flow rate did not affect the angle threshold of 85°, past which positive WSSG occurs. In curved models, high flow displaced the impingement area away from the apex, in a dynamic fashion and in an angle-dependent manner.CONCLUSIONSApical shear forces and spatial gradients are highly dependent on bifurcation and inflow vessel geometry. The development of aneurysmogenic positive WSSG as a function of angular geometry provides a mechanotransductive link for the association of wide bifurcations and aneurysm development. These results suggest therapeutic strategies aimed at altering underlying unfavorable geometry and deciphering the molecular endothelial response to shear gradients in a bid to disrupt the associated aneurysmal degeneration.


1995 ◽  
Vol 117 (3) ◽  
pp. 350-357 ◽  
Author(s):  
M. Lei ◽  
C. Kleinstreuer ◽  
G. A. Truskey

Atherosclerosis, a disease of large- and medium-size arteries, is the chief cause of death in the US and most of the western world. It is widely accepted that the focal nature of the disease in arterial bends, junctions, and bifurcations is directly related to locally abnormal hemodynamics, often labeled “disturbed flows.” Employing the aorto-celiac junction of rabbits as a representative atherosclerotic model and considering other branching blood vessels with their distinctive input wave forms, it is suggested that the local wall shear stress gradient (WSSG) is the single best indicator of nonuniform flow fields leading to atherogenesis. Alternative predictors of susceptible sites are briefly evaluated. The results discussed include transient velocity vector fields, wall shear stress gradient distributions, and a new dimensionless parameter for the prediction of the probable sites of stenotic developments in branching blood vessels. Some of the possible underlying biological aspects of atherogenesis due to locally significant |WSSG|-magnitudes are briefly discussed.


Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard Leask

Endothelial cell (EC) dysfunction has been linked to atherosclerosis through their response to hemodynamic forces. Flow in stenotic vessels creates complex spatial gradients in wall shear stress. In vitro studies examining the effect of shear stress on endothelial cells have used unrealistic and simplified models, which cannot reproduce physiological conditions. The objective of this study was to expose endothelial cells to the complex shear shear pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flow in straight dynamic controls and in idealized asymmetric stenosis models. Cells subjected to 1D flow aligned with flow direction and had a spindle-like shape when compared to static controls. Endothelial cell morphology was noticeable different in the regions with a spatial gradient in wall shear stress, being more randomly oriented and of cobblestone shape. This occurred despite the presence of an increased magnitude in shear stress. No other study to date has described this morphology in the presence of a positive wall shear stress gradient or gradient of significant shear magnitude. This technique provides a more realistic model to study endothelial cell response to spatial and temporal shear stress gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.


2016 ◽  
Vol 10 (5) ◽  
pp. 054119 ◽  
Author(s):  
Hyung Woo Kim ◽  
Seonjin Han ◽  
Wonkyoung Kim ◽  
Jiwon Lim ◽  
Dong Sung Kim

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Michael McElroy ◽  
Yongcheol Kim ◽  
Giampaolo Niccoli ◽  
Rocco Vergallo ◽  
Alexander Langford-Smith ◽  
...  

AbstractEndothelial erosion of atherosclerotic plaques is the underlying cause of approximately 30% of acute coronary syndromes (ACS). As the vascular endothelium is profoundly affected by the haemodynamic environment to which it is exposed, we employed computational fluid dynamic (CFD) analysis of the luminal geometry from 17 patients with optical coherence tomography (OCT)-defined plaque erosion, to determine the flow environment permissive for plaque erosion. Our results demonstrate that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (interquartile range 28–52%), where all but one of the adherent thrombi located proximal to, or within the region of maximum stenosis. Consequently, all flow metrics related to elevated flow were significantly increased (time averaged wall shear stress, maximum wall shear stress, time averaged wall shear stress gradient) with a reduction in relative residence time, compared to a non-diseased reference segment. We also identified two cases that did not exhibit an elevation of flow, but occurred in a region exposed to elevated oscillatory flow. Our study demonstrates that the majority of OCT-defined erosions occur where the endothelium is exposed to elevated flow, a haemodynamic environment known to evoke a distinctive phenotypic response in endothelial cells.


2011 ◽  
Vol 32 (3) ◽  
pp. 587-594 ◽  
Author(s):  
Z. Kulcsár ◽  
Á. Ugron ◽  
M. Marosfői ◽  
Z. Berentei ◽  
G. Paál ◽  
...  

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