Design and construction of a linear shear stress flow chamber

1993 ◽  
Vol 21 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Shunichi Usami ◽  
Hsuan-Hsu Chen ◽  
Yihua Zhao ◽  
Shu Chien ◽  
Richard Skalak
2018 ◽  
Vol 140 (6) ◽  
Author(s):  
Hamed Avari ◽  
Kem A. Rogers ◽  
Eric Savory

The parallel plate flow chamber (PPFC) has gained popularity due to its applications in fields such as biological tissue engineering. However, most of the studies using PPFC refer to theoretical relations for estimating the wall shear stress (WSS) and, hence, the accuracy of such quantifications remains elusive for anything other than steady laminar flow. In the current study, a laser Doppler velocimetry (LDV) method was used to quantify the flow in a PPFC (H = 1.8 mm × W = 17.5 mm, Dh = 3.26 mm, aspect ratio = 9.72) under steady Re = 990, laminar pulsatile (carotid Re0-mean = 282 as well as a non-zero-mean sinusoidal Re0-mean = 45 pulse) and low-Re turbulent Re = 2750 flow conditions. A mini-LDV probe was applied, and the absolute location of the LDV measuring volume with the respect to the wall was determined using a signal monitoring technique with uncertainties being around ±27 μm. The uniformity of the flow across the span of the channel, as well as the WSS assessment for all the flow conditions, was measured with the uncertainties all being less than 16%. At least two points within the viscous sublayer of the low-Re turbulent flow were measured (with the y+ for the first point < 3) and the WSS was determined using two methods with the differences between the two methods being within 5%. This paper for the first time presents the experimental determination of WSS using LDV in a small-scale PPFC under various flow conditions, the challenges associated with each condition, and a comparison between the cases. The present data will be useful for those conducting biological or numerical modeling studies using such devices.


2000 ◽  
Vol 89 (4) ◽  
pp. 1657-1662 ◽  
Author(s):  
Chauying J. Jen ◽  
Shuo-Ju Jhiang ◽  
Hsiun-Ing Chen

To study the effects of flow on in situ endothelial intracellular calcium concentration ([Ca2+]i) signaling, rat aortic rings were loaded with fura 2, mounted on a tissue flow chamber, and divided into control and flow-pretreated groups. The latter was perfused with buffer at a shear stress of 50 dyns/cm2 for 1 h. Endothelial [Ca2+]i responses to ACh or shear stresses were determined by ratio image analysis. Moreover, ACh-induced [Ca2+]i elevation responses were measured in a calcium-free buffer, or in the presence of SKF-96365, to elucidate the role of calcium influx in the flow effects. Our results showed that 1) ACh increased endothelial [Ca2+]i in a dose-dependent manner, and these responses were incremented by flow-pretreatment; 2) the differences in ACh-induced [Ca2+]i elevation between control and flow-pretreated groups were abolished by SKF-96365 or by Ca2+-free buffer; and 3) in the presence of 10−5 M ATP, shear stress induced dose-dependent [Ca2+]i elevation responses that were not altered by flow-pretreatment. In conclusion, flow-pretreatment augments the ACh-induced endothelial calcium influx in rat aortas ex vivo.


2004 ◽  
Vol 287 (3) ◽  
pp. H994-H1002 ◽  
Author(s):  
Akinori Ueda ◽  
Masaki Koga ◽  
Mariko Ikeda ◽  
Susumu Kudo ◽  
Kazuo Tanishita

Shear stress stimulus is expected to enhance angiogenesis, the formation of microvessels. We determined the effect of shear stress stimulus on three-dimensional microvessel formation in vitro. Bovine pulmonary microvascular endothelial cells were seeded onto collagen gels with basic fibroblast growth factor to make a microvessel formation model. We observed this model in detail using phase-contrast microscopy, confocal laser scanning microscopy, and electron microscopy. The results show that cells invaded the collagen gel and reconstructed the tubular structures, containing a clearly defined lumen consisting of multiple cells. The model was placed in a parallel-plate flow chamber. A laminar shear stress of 0.3 Pa was applied to the surfaces of the cells for 48 h. Promotion of microvessel network formation was detectable after ∼10 h in the flow chamber. After 48 h, the length of networks exposed to shear stress was 6.17 (±0.59) times longer than at the initial state, whereas the length of networks not exposed to shear stress was only 3.30 (±0.41) times longer. The number of bifurcations and endpoints increased for networks exposed to shear stress, whereas the number of bifurcations alone increased for networks not exposed to shear stress. These results demonstrate that shear stress applied to the surfaces of endothelial cells on collagen gel promotes the growth of microvessel network formation in the gel and expands the network because of repeated bifurcation and elongation.


1993 ◽  
Vol 265 (1) ◽  
pp. H3-H8 ◽  
Author(s):  
M. Mitsumata ◽  
R. S. Fishel ◽  
R. M. Nerem ◽  
R. W. Alexander ◽  
B. C. Berk

Fluid flow and the associated shear stress play a critical role in vascular growth and remodeling. Recent data suggest that increased endothelial cell expression of platelet-derived growth factor (PDGF) A- and B-chain by flow may participate in these events. In the present study, we examined the mechanism for flow-induced PDGF expression, focusing on protein kinase C (PKC). Bovine aortic endothelial cells were exposed to flow (shear stress = 30 dyn/cm2) in a parallel-plate flow chamber. Increases in PDGF B-chain, but not PDGF A-chain, were observed within 3 h, maximal within 6 h (13-fold increase), and sustained for 24 h. PKC appeared to be involved because phorbol 12-myristate 13-acetate induced PDGF B-chain mRNA. Activation of PKC alone, however, was insufficient to induce PDGF mRNA because the selective PKC activator, 1-oleoyl-2-acetyl-sn-glycerol, did not induce PDGF expression. A PKC-independent pathway was suggested by the fact that inhibition of PKC (downregulation with phorbol 12,13-dibutyrate or exposure to staurosporine) failed to block PMA or flow-induced PDGF B-chain expression. These results demonstrate flow-induced PDGF B-chain expression in endothelial cells that appears to be mediated, in part, by a PKC-independent pathway.


Nanoscale ◽  
2018 ◽  
Vol 10 (32) ◽  
pp. 15249-15261 ◽  
Author(s):  
M. Juliana Gomez-Garcia ◽  
Amber L. Doiron ◽  
Robyn R. M. Steele ◽  
Hagar I. Labouta ◽  
Bahareh Vafadar ◽  
...  

Hemodynamic factors drive nanoparticle distribution in vivo and in vitro in cell-based flow models.


2015 ◽  
Vol 27 (05) ◽  
pp. 1550042 ◽  
Author(s):  
Jen-Hong Yen ◽  
Sheng-Fu Chen ◽  
Ming-Kai Chern ◽  
Po-Chien Lu

Artificial prostheses create non-physiologic flow conditions with stress forces that may induce blood cell damage, particularly hemolysis. Earlier computational fluid dynamics (CFD) prediction models based on a quantified power model showed significant discrepancies with actual hemolysis experiments. These models used the premise that shear stresses act as the primary force behind hemolysis. However, additional studies have suggested that extensional stresses play a more substantial role than previously thought and should be taken into account in hemolysis models. We compared extensional and shear stress flow fields within the contraction of a short capillary with sharp versus tapered entrances. The flow field was calculated with CFD to determine stress values, and hemolysis experiments with porcine red blood cells were performed to correlate the effects of extensional and shear stress on hemolysis. Our results support extensional stress as the primary mechanical force involved in hemolysis, with a threshold value of 1000 Pa under exposure time less than 0.060 ms.


1985 ◽  
Vol 107 (4) ◽  
pp. 341-347 ◽  
Author(s):  
M. J. Levesque ◽  
R. M. Nerem

Vascular endothelial cells appear to be aligned with the flow in the immediate vicinity of the arterial wall and have a shape which is more ellipsoidal in regions of high shear and more polygonal in regions of low shear stress. In order to study quantitatively the nature of this response, bovine aortic endothelial cells grown on Thermanox plastic coverslips were exposed to shear stress levels of 10, 30, and 85 dynes/cm2 for periods up to 24 hr using a parallel plate flow chamber. A computer-based analysis system was used to quantify the degree of cell elongation with respect to the change in cell angle of orientation and with time. The results show that (i) endothelial cells orient with the flow direction under the influence of shear stress, (ii) the time required for cell alignment with flow direction is somewhat longer than that required for cell elongation, (iii) there is a strong correlation between the degree of alignment and endothelial cell shape, and (iv) endothelial cells become more elongated when exposed to higher shear stresses.


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