High Levels Of Shear Stress Research Articles

The study of wall deformation and flow distribution with transmural pressure by three-dimensional model of thoracic aorta wall

The sensitivity of shear stress over smooth muscle cells (SMCs) to the deformability of media layer due to pressure is investigated in thoracic aorta wall using three-dimensional simulations. A biphasic, anisotropic model assuming the radius, thickness, and hydraulic conductivity of vessel wall as functions of transmural pressure is employed in numerical simulations. The leakage of interstitial fluid from intima to media layer is only possible through fenestral pores on the internal elastic lamina (IEL). The media layer is assumed a heterogeneous medium containing SMCs embedded in a porous extracellular matrix of elastin, proteoglycan, and collagen fibers. The applicable pressures for the deformation of media layer are varied from 0 to 180 mmHg. The SMCs are cylindrical objects of circular cross section at zero pressure. The cross sectional shape of SMCs changes from circle to ellipse as the media is compressed. The local shear stress over the nearest SMC to the IEL profoundly depends on pressure, SMCs configurations, and the corresponding distance to the IEL. The consideration of various SMC configurations, namely the staggered and square arrays, mimics various physiological conditions that can happen in positioning of an SMC. The results of our simulations show that even the second nearest SMCs to the IEL can significantly change their functions due to high shear stress levels. This is in contrast to earlier studies suggesting the highest vulnerability to shear stress for the innermost layer of SMCs at the intimal-medial interface.

Platelets undergo phosphorylation of Syk at Y525/526 and Y352 in response to pathophysiological shear stress

Atherosclerotic plaques can lead to partial vascular occlusions that produce abnormally high levels of arterial wall shear stress. Such pathophysiological shear stress can promote shear-induced platelet aggregation (SIPA), which has been linked to acute myocardial infarction, unstable angina, and stroke. This study investigated the role of the tyrosine kinase Syk in shear-induced human platelet signaling. The extent of Syk tyrosine phosphorylation induced by pathophysiological levels of shear stress (100 dyn/cm(2)) was significantly greater than that resulting from physiological shear stress (10 dyn/cm(2)). With the use of phospho-Syk specific antibodies, these data are the first to show that key regulatory sites of Syk at tyrosines 525/526 (Y525/526) and tyrosine 352 (Y352) were phosphorylated in response to pathophysiological shear stress. Increased phosphorylation at both sites was attenuated by pharmacological inhibition of Syk using two different Syk inhibitors, piceatannol and 3-(1-methyl-1H-indol-3-yl-methylene)-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide (OXSI-2), and by inhibition of upstream Src-family kinases (SFKs). Shear-induced response at the Syk 525/526 site was ADP dependent but not contingent on glycoprotein (GP) IIb-IIIa ligation or the generation of thromboxane (Tx) A(2). Pretreatment with Syk inhibitors not only reduced SIPA and Syk phosphorylation in isolated platelets, but also diminished, up to 50%, the platelet-mediated thrombus formation when whole blood was perfused over type-III collagen. In summary, this study demonstrated that Syk is a key molecule in both SIPA and thrombus formation under flow. Pharmacological regulation of Syk may prove efficacious in treating occlusive vascular disease.

The elusive lithosphere–asthenosphere boundary (LAB) beneath cratons

The lithosphere–asthenosphere boundary (LAB) is a first-order structural discontinuity that accommodates differential motion between tectonic plates and the underlying mantle. Although it is the most extensive type of plate boundary on the planet, its definitive detection, especially beneath cratons, is proving elusive. Different proxies are used to demarcate the LAB, depending on the nature of the measurement. Here we compare interpretations of the LAB beneath three well studied Archean regions: the Kaapvaal craton, the Slave craton and the Fennoscandian Shield. For each location, xenolith and xenocryst thermobarometry define a mantle stratigraphy, as well as a steady-state conductive geotherm that constrains the minimum pressure (depth) of the base of the thermal boundary layer (TBL) to 45–65 kbar (170–245 km). High-temperature xenoliths from northern Lesotho record Fe-, Ca- and Ti-enrichment, grain-size reduction and globally unique supra-adiabatic temperatures at 53–61 kbar (200–230 km depth), all interpreted to result from efficient advection of asthenosphere-derived melts and heat into the TBL. Using a recently compiled suite of olivine creep parameters together with published geotherms, we show that beneath cratons the probable deformation mechanism near the LAB is dislocation creep, consistent with widely observed seismic and electrical anisotropy fabrics. If the LAB is dry, it is probably diffuse (> 50 km thick) and high levels of shear stress (> 2 MPa or > 20 bar) are required to accommodate plate motion. If the LAB is wet, lower shear stress is required to accommodate plate motion and the boundary may be relatively sharp (≤ 20 km thick). The seismic LAB beneath cratons is typically regarded as the base of a high-velocity mantle lid, although some workers infer its location based on a distinct change in seismic anisotropy. Surface-wave inversion studies provide depth-constrained velocity models, but are relatively insensitive to the sharpness of the LAB. The S-receiver-function method is a promising new seismic technique with complementary characteristics to surface-wave studies, since it is sensitive to sharpness of the LAB but requires independent velocity information for accurate depth estimation. Magnetotelluric (MT) observations have, for many decades, imaged an “electrical asthenosphere” layer at depths beneath the continents consistent with seismic low-velocity zones. This feature is most easily explained by the presence of a small amount of water in the asthenosphere, possibly inducing partial melt. Depth estimates based on various proxies considered here are similar, lending confidence that existing geophysical tools are effective for mapping the LAB beneath cratons.

Coherent Structures in the Flow Field around a Circular Cylinder with Scour Hole

Large-eddy simulation (LES) and laboratory-flume visualizations were used to investigate coherent structures present in the flow field around a circular cylinder located in a scour hole. The bathymetry corresponds to equilibrium scour conditions and is fixed in LES. The flow parameters in the simulation correspond to the experimental conditions in which the approach flow is fully turbulent. Detailed consideration is given to the interaction of the horseshoe vortex (HV) system within the scour hole with the detached shear layers formed from the cylinder, and the near bed turbulence. It is found that the overall structure of the HV system varies considerably in space and time, though a large, relatively stable, primary necklace vortex is present at practically all times inside the scour hole. The simulation captures the presence of bimodal chaotic oscillations inside the HV system, as well as the sharp increase in the resolved turbulent kinetic energy levels and pressure fluctuations reported in prior experimental investigations. High levels of the mean bed shear stress are observed beneath the primary necklace vortex, especially over the region where the bimodal oscillations are strong, as well as beneath the small junction vortex at the base of the cylinder. It is also found that the detachment and advection of patches of vorticity from the downstream part of the legs of the necklace vortices can induce large instantaneous bed shear stress values. When the critical bed shear stress value for sediment entrainment on a flat surface is adjusted for bed slope effects, the LES simulation correctly predicts that the distribution of the mean bed shear stress is consistent with equilibrium scour conditions.

Modelling of Ageing Effects on the Elasto-Viscoplastic Behaviour of Geomaterial

The time effects on the stress-strain behaviour of geomaterial consist of effects of loading rate and ageing. The positive ageing effects are analysed based on the results from drained triaxial compression (TC) tests on cement-mixed kaolin and well-graded gravelly soil and incorporated into a non-linear three-component model that can simulate the elasto-viscoplastic behaviour of geomaterials. The inviscid yielding is controlled by the inviscid yield stress that develops basically by irreversible straining and time elapsing following, respectively, a basic inviscid strain-hardening function and an ageing function. The inviscid yield stress may develop additionally by positive interaction between ageing and inviscid yielding following an interaction function, which expresses an additional strength gain by longer ageing at higher shear stress levels. Positive interaction effects are damaged by subsequent irreversible straining following a damage function. These functions are formulated based on experimental results. Illustrative model simulations are presented to describe the structure of the proposed model. The model is validated by simulating drained TC tests exhibiting significant effects of loading rate and ageing.

Pavement Rutting Performance Prediction by Integrated Weibull Approach

This paper demonstrates the applicability of the integrated Weibull approach to simulate the in situ rutting performance of asphalt concrete mixes by applying appropriate correction factors to laboratory models. The goal was to verify and calibrate the laboratory models according to accelerated pavement test results. The results of the repeated simple shear test at constant height (RSST-CH) were used to estimate the permanent deformation accumulation mechanisms. General regression equations were shown to successfully represent the Stage I and Stage II permanent deformation accumulation phases for mixes containing different binder types according to the results of RSST-CH. Correction factors were used to calibrate the laboratory equations according to the deflection data from four heavy vehicle simulator test sections to estimate in situ rutting performance. The results indicate that phase separation occurs at higher repetition values with increasing shear stress. Moreover, only Stage I of the laboratory models was actually valid at the high shear stress levels used for in situ rutting performance prediction. The simulations further confirm that the integrated Weibull approach is a successful and reliable method for prediction of the in situ rutting performance of flexible pavements and provides high coefficient of determination values.

Rapamycin modulates the eNOS vs. shear stress relationship

Studies in animals and patients indicate that rapamycin affects vasodilatation differently in outer and inner curvatures of blood vessels. We evaluated in this study whether rapamycin affects endothelial nitric oxide synthase (eNOS) responsiveness to shear stress under normo- and hypercholesteraemic conditions to explain these findings. Shear stress levels were varied over a large range of values in carotid arteries of transgenic mice expressing human eNOS fused to enhanced green fluorescence protein. The mice were divided into control, low-dose rapamycin (3 microg/kg/day), and high-dose rapamycin (3 mg/kg/day) groups and into normocholesteraemic and hypercholesteraemic (ApoE-/- on high cholesterol diet for 3-4 weeks) groups. The effect of rapamycin treatment on eNOS was evaluated by quantification of eNOS expression and of intracellular protein levels by en face confocal microscopy. A sigmoid curve fit was used to described these data. The efficacy of treatment was confirmed by measurement of rapamycin serum levels (2.0 +/- 0.5 ng/mL), and of p27kip1 expression in vascular tissue (increased by 2.4 +/- 0.5-fold). In control carotid arteries, eNOS expression increased by 1.8 +/- 0.3-fold in response to rapamycin. In the treated vessels, rapamycin reduced maximal eNOS expression at high shear stress levels (>5 Pa) in a dose-dependent way and shifted the sigmoid curve to the right. Hypercholesteraemia had a tendency to increase the leftward shift and the reduction in maximal eNOS expression (P = 0.07). Rapamycin is associated with high eNOS in low shear regions, i.e. in atherogenic regions, protecting these regions against atherosclerosis, and is associated with a reduction of eNOS at high shear stress affecting vasomotion in these regions.

Vasculoprotective properties of the endothelial glycocalyx: effects of fluid shear stress

The endothelial glycocalyx exerts a wide array of vasculoprotective effects via inhibition of coagulation and leucocyte adhesion, by contributing to the vascular permeability barrier and by mediating shear stress-induced NO release. In this review, we will focus on the relationship between fluid shear stress and the endothelial glycocalyx. We will address the hypothesis that modulation of glycocalyx synthesis by fluid shear stress may contribute to thinner glycocalyces, and therefore more vulnerable endothelium, at lesion-prone sites of arterial bifurcations. Finally, we will discuss the effects of known atherogenic stimuli such as hyperglycaemia on whole body glycocalyx volume in humans and its effect on endothelial function.

Time-Dependent Rheological Behavior of Liquid Crystalline Dispersions

The rheological response of Aerosol OT (AOT)/water liquid crystalline dispersions is reported here using shear flows. The dispersions exhibit an apparent yield stress and strong non-Newtonian behavior. Steady state and pre-shear dynamical experiments reveal shear-induced structural changes. Under increasing-and-decreasing shear stress experiments, the dispersions exhibit anti-thixotropic hysteresis loops. Once a critical stress is surpassed, an additional thixotropic loop is observed at high shear stress levels. This inverse loop at high shear stresses depends on the previous shear history and on both the rate of change and the maximum attained value of shear stress. The number density of the globular structures in the sheared sample is larger than in one non-sheared sample, but their sizes are smaller than those of the non-sheared sample.

A Statistical Method to Evaluate the Effect of Shear Stress on Endothelial Gene Expression in vivo

Objective To determine the effect of hemodynamic shear stress on endothelial gene expression in vivo. Methods Computational fluid dynamics (CFD) simulations were performed in three realistic models of the porcine abdominal aorta and its iliac artery branches. Using these calculations, a shear stress probability map in the iliac arteries was generated. This map showed the likelihood that a particular location would experience high, medium, or low time average shear stress. Based on this map, three anatomical regions likely to experience high, medium, and low shear stress levels were identified. The median time-average shear stress in these regions were 32.1, 15.2, and 9.7 dyn/cm2, respectively. Subsequently, endothelial cell RNA was collected from these regions in five additional porcine iliac arteries. Gene expression of select genes was measured in these samples using quantitative real time PCR. Results for the high and low shear regions are reported relative to the medium shear region. Results Expression of the genes tubulin, beta-catenin, c-jun, MCP-1, and VCAM was elevated in both the low and high shear stress regions relative to the medium shear region. ICAM expression was downregulated in both the low and high shear regions relative to the medium shear region. These effects were significant in nearly all cases. Conclusions This statistical method permits evaluation of phenotypic differences that arise due to hemodynamic forces in in vivo specimens. Arterial regions subjected to distinct levels of time average shear stress exhibit differences in endothelial gene expression. Supported by NIH grant H50442.

Mechanisms of Endothelial Cell Heterogeneity in Health and Disease

See related article, pages 200–208 The endothelium is an expansive spatially distributed organ.1 Endothelial cells participate in a large number of physiological processes including the control of vasomotor tone, the trafficking of cells and nutrients, the regulation of permeability, and the maintenance of blood fluidity. In addition, the endothelium mediates new blood vessel formation, contributes to the balance of pro- and antiinflammatory mediators, and may play a role in antigen presentation. In accomplishing these tasks, the endothelium exhibits a remarkable “division of labor”. For example, arteriolar endothelium is primarily responsible for mediating vasomotor tone; endothelium in postcapillary venules regulates leukocyte trafficking; capillary endothelial cells display organ-specific barrier properties (eg, blood brain barrier versus fenestrated, discontinuous endothelium in hepatic sinusoids); and endothelial cells from different vascular beds balance local hemostasis via the expression of site-specific patterns of anticoagulants and procoagulants.2 In recent years, in vivo phage display and direct proteome mapping of the intact vasculature have revealed a rich diversity in endothelial cell surface markers.3,4 Any consideration of the mechanisms underlying endothelial heterogeneity is best framed around the time-honored debate of nature versus nurture (which will be addressed here in reverse order) (Figure). Mechanisms of endothelial cell heterogeneity. Relative importance of epigenetics and microenvironment in mediating site-specific phenotypes is indicated by +. The table is designed to provide a conceptual framework; the scores are largely speculative and will require ongoing experimental validation. ### Nurture Site-specific endothelial cell phenotypes may be initiated and maintained by signals residing in the extracellular environment. The endothelium is analogous to a barcode reader, constantly taking inventory of its surrounding extracellular environment on the luminal side (circulating blood and its constituents), the abluminal side, and at the endothelial junctions. Environmental cues may be classified into biomechanical or biochemical. Biochemical forces include shear stress and strain. …

Age-associated impairment in vasorelaxation to fluid shear stress in the female vasculature is improved by TNF-α antagonism

Aging is associated with alterations in vascular homeostasis, including a reduction in flow-mediated vasodilation, which in women is related to the onset of menopause. We previously found that in female animals, aging is associated with an increase in TNF-alpha. Thus we investigated the role of in vivo TNF-alpha inhibition on vascular responses to shear stress in aging female rats. Mesenteric arteries (approximately 150 microm) were isolated from young (3 mo) and ovariectomized Sprague-Dawley female rats approaching reproductive senescence (12 mo) treated with either placebo or a TNF-alpha inhibitor (etanercept; 0.3 mg/kg) and were mounted on a pressure myograph system. Vessels were equilibrated at an intraluminal pressure of 60 mmHg and then preconstricted with phenylephrine at approximately 70% of their initial diameter. Perfusate flow was increased in steps from 0 to 150 microl/min. Compared with young vessels, aged vessels have a decrease in flow-mediated dilation [maximal dilation (means +/- SE): 52 +/- 4 vs. 24 +/- 15%; P < 0.05], which was improved by TNF-alpha inhibition. Moreover, in aged vessels maximal dilation to flow was achieved at higher levels of shear stress compared with young vessels. In all groups, flow-mediated dilation was abolished by either endothelial removal or nitric oxide synthase inhibition with N(G)-nitro-L-arginine methyl ester. However, the modulation by N(G)-nitro-L-arginine methyl ester was reduced in vessels from aged animals compared with young animals but was improved in the etanercept-treated aged animals. In vivo chronic TNF-alpha inhibition improves flow-mediated arterial dilation in resistance arteries of aged female animals.

Monocilia on chicken embryonic endocardium in low shear stress areas

During cardiovascular development, fluid shear stress patterns change dramatically due to extensive remodeling. This biomechanical force has been shown to drive gene expression in endothelial cells and, consequently, is considered to play a role in cardiovascular development. The mechanism by which endothelial cells sense shear stress is still unidentified. In this study, we postulate that primary cilia function as fluid shear stress sensors of endothelial cells. Such a function already has been attributed to primary cilia on epithelial cells of the adult kidney and of Hensen's node in the embryo where they transduce mechanical signals into an intracellular Ca2+ signaling response. Recently, primary cilia were observed on human umbilical vein endothelial cells. These primary cilia disassembled when subjected to high shear stress levels. Whereas endocardial-endothelial cells have been reported to be more shear responsive than endothelial cells, cilia are not detected, thus far, on endocardial cells. In the present study, we use field emission scanning electron microscopy to show shear stress-related regional differences in cell protrusions within the cardiovasculature of the developing chicken. Furthermore, we identify one of these cell protrusions as a monocilium with monoclonal antibodies against acetylated and detyrosinated alpha-tubulin. The distribution pattern of the monocilia was compared to the chicken embryonic expression pattern of the high shear stress marker Krüppel-like factor-2. We demonstrate the presence of monocilia on endocardial-endothelial cells in areas of low shear stress and postulate that they are immotile primary cilia, which function as fluid shear stress sensors.

Why Do We Need ADAMTS13?

ADAMTS13 is a member of a newly recognized zinc metalloprotease family that has been the subject of intense interest in recent years. Cleavage of von Willebrand factor by this protease is essential for preventing the development of thrombotic thrombocytopenic purpura (TTP) Von Willebrand factor (VWF), synthesized in vascular endothelial cells and megakaryocytes, supports platelet adhesion and aggregation at sites of vessel injury under high shear stress conditions. VWF exists in the circulation as a series of multimers, which were once believed to be released directly from vascular endothelial cells. By late 1980’s, much was known about the physiology and genetics of VWF. Nevertheless, three characteristics of VWF-platelet interaction in hemostasis had resisted efforts to unravel their molecular mechanisms (Table 1). First, VWF-platelet binding occurs only at sites of vessel injury but not in the circulation. There are two receptors on platelet surface that are engaged in VWF binding: glycoproteins αIIbβ3 and Ib/IX/V. Much is known about the regulation of VWF–αIIbβ3: αIIbβ3, normally in an inactive conformation, is transformed upon platelet activation to a competent form for ligand binding. In contrast, the regulation of VWF–Ib/IX/V remained mostly unclear. There is no definitive evidence that Ib/IX/V requires activation. What processes prevent VWF-platelet binding in the circulation but allows it to occur at sites of vessel injury? Second, several lines of evidence suggest that the large VWF multimers arc hemostatically more effective than small multimers. What is the molecular basis of this size dependence? Third, in experimental models, high levels of shear stress enhance the VWF-mediated platelet aggregation. What are the molecular features of VWF that enable VWF to become more effective under high shear stress conditions? Table 1 Characteristics of VWF-platelel interaction and their causes

NCHRP Project 12-61, Simplified Shear Design of Structural Concrete Members

A new method of shear design was introduced into the U.S. community with the AASHTO LRFD Bridge Design Specifications. This method, which is based on the modified compression field theory, provides a unified approach for the shear design of both prestressed and nonprestressed members, overcomes a number of safety concerns, and enables members to be designed for higher shear stress levels. Unfortunately, this design methodology is perceived by many as being more complex than AASHTO's standard specifications. To address this concern, NCHRP funded Project 12-61, Simplified Shear Design of Structural Concrete Members. The objective of this project was to supplement the full LRFD method for shear design with a simplified procedure that provides a direct solution for transverse and longitudinal reinforcement of concrete structures of common proportions. The research approach was to establish the simplified provisions after a rigorous assessment of the merits and limitations of existing shear design methodologie...

Estimation of Melt Shear Modulus from Extrudate Swell Ratio and Exit-pressure Drop Data

Obvious viscoelastic phenomena, such as die-swell and exit-pressure losses, appear when a viscoelastic fluid leaves a die. It is generally believed that the die-swell ratio (B), the melt shear modulus (G), and the exit-pressure drop (Δ Pex) are important parameters for the characterization of the elastic behavior of viscoelastic fluids during die flow. There may be, therefore, some interrelations between them. In the present article, relationships among G, B, and Δ Pex are discussed. On the basis of previous work, some expressions for describing relationships between B and G, Δ Pex, and B, as well as Δ Pex and G during flow of viscoelastic fluids in a long circular die are proposed. The values of G are estimated from the measured B during extrusion of a carbon black and calcium carbonate-filled rubber compound, and predictions of G by using the measured data of Δ Pex are compared with its calculations from the B data during capillary extrusion of a high-density polyethylene (HDPE) melt. The results showed that G increases linearly with increasing shear stress. Furthermore, a good agreement was obtained among these theoretical calculations of G at high shear stress level, also being consistent with predictions by using the Bagley-Duffey equation.

A Tensor‐based Measure for Estimating Blood Damage

Implantable ventricular assist devices give hope of a permanent clinical solution to heart failure. These devices, both pulsatile- and continuous-flow, are presently used as medium-term bridge to heart transplant or recovery. While long-term use of continuous-flow axial and centrifugal pumps is being explored, the excessive level of blood damage in these devices has emerged as a design challenge. Blood damage depends both on shear stress and exposure time, and device designers have relied traditionally on global space- and time-averaged estimates from experimental studies to make design decisions. Measuring distributions of shear stress levels and the blood cell's exposure to these conditions in complex rotary pump flow is difficult. On the other hand, computational fluid dynamics (CFD) is now being used as a tool for designing viable devices, offering more detailed information about the flow field. A tensor-based blood damage model for CFD analysis is proposed here. The model estimates the time- and space-dependent strain experienced by individual blood cells and correlates it to blood damage data from steady shear flow experiments. The blood cells are modeled as deforming droplets and their deformation is tracked along the pathlines of a computed flow. The model predicts that blood cells in a rapidly fluctuating shear flow can sustain high shear stress levels for very short exposure time without deforming considerably. In the context of mechanical modeling of the implantable Gyro blood pump being developed at Baylor College of Medicine, this suggests that blood cells traversing regions of highly fluctuating shear stress rapidly may not hemolyze significantly.

Chondrocyte senescence, joint loading and osteoarthritis.

cellular level is not completely understood, but both aging and loading-induced stresses have been shown to undermine cell functions related to the maintenance and restoration of the cartilage matrix. Based on precedents set by studies of other age-related degenerative diseases, we have focused our laboratory work on senescence as the cause of age-dependent decline in chondrocytes and on the impact of excessive mechanical stresses in promoting senescence. We hypothesized that senescent chondrocytes accumulate with age in articular cartilage and we propose that excessive mechanical stress plays a role in this process by promoting oxidative damage in chondrocytes that ultimately causes them to senesce. To test this hypothesis, we measured cell senescence markers (beta-galactosidase expression, mitotic activity, and telomere length) in human articular cartilage chondrocytes, and determined the effects of chronic exposure to oxidative stress on chondrocyte growth and senescence. In addition, we measured the effects of abnormally high levels of mechanical shear stress on the release of oxidants in cartilage explants. We found that senescent chondrocytes accumulated with age in articular cartilage. In vitro studies showed that chronic oxidative stress caused by repeated exposure to peroxide, or by growth under superphysiologic oxygen tension caused chondrocyte populations to senesce prematurely, before extensive telomere erosion occurred. Mechanical shear stress applied to cartilage explants considerably increased the production of oxidants. These observations support the hypothesis that senescence accounts for age-related decline in chondrocyte function and indicate that mechanically induced oxidative damage plays a role in this process. This suggests that new efforts to prevent the development and progression of osteoarthritis should include strategies that slow the progression of chondrocyte senescence or replace senescent cells.

Flow pattern and shear stress distribution of distal end-to-side anastomoses. A comparison of the instantaneous velocity fields obtained by particle image velocimetry

Objective: To describe the local hemodynamics and pressure losses of crural bypass anastomoses using instantaneous velocity fields acquired by particle image velocimetry (PIV). Methods: Silastic models of a Taylor patch, a Miller cuff and a femoro-crural patch prosthesis (FCPP) were attached to a circuit driven by a Berlin Heart, providing a pulsatile flow with an amplitude of 450 to 25 ml/min (mean 200 ml/min). An outflow resistance of 0.5 mmHg/ml/min (peripheral resistance units, PRU) was modeled using small silastic tubes providing a phase shift of −12° between flow and pressure curves. The working fluid consisted of a glycerine/water mixture with a viscosity of 4 mPa s. Hollow glass spheres with a mean size of 9–13 μm were used as tracer particles. Instantaneous velocity fields were obtained by means of PIV and shear rates as well as shear stresses were calculated. Triggered by the flowmeter signal, 10 measurements at 100 ms intervals per cardiac cycle were obtained. The pressures were measured on the inflow and at both distal outflows. The resulting mean pressure losses due to flow separation and distal fluid acceleration were calculated. Results: Inside the Taylor patch anastomosis a large flow separation at the hood containing a clockwise rotating vortex was found. Additionally a smaller flow separation at the heel and a flow stagnation zone on the floor of the recipient artery were observed. Conversely, inside the Miller cuff a counterclockwise rotating vortex was seen inside a large heel flow separation. The FCPP also showed typical separation areas at the hood and heel of the anastomosis, although these were smaller compared to the other anastomoses. Inside the FCPP anastomosis no vortex creation was observed throughout the cardiac cycle. The mainstream velocities at the inlet levels were comparable for the three anastomoses. A significant fluid acceleration was present at the antegrade as well as the retrograde outlets of the Taylor and Miller cuff, while the fluid acceleration at the antegrade outflow of the FCPP was small, which was attributed to the end-to-end configuration of the antegrade FCPP leg. The calculated normalized antegrade and retrograde pressure losses for the Taylor form were 0.90 and 0.88, for the Miller cuff 0.89 and 0.86 and for the FCPP 0.94 and 0.86, respectively. The shear stresses inside the flow separations of the three anastomoses were significantly lower than normal wall shear stresses. High shear stress levels were found inside the transition zones between flow separation and high velocity mainstream. Conclusions: The flow pattern inside cuffed or funnel shaped anastomoses consists of large flow separation zones, which are thought to be associated with intimal hyperplasia development. In addition, fluid accelerations at the distal outlets result in pressure losses, which may contribute to impaired crural perfusion.

Floc morphology and size distributions of cohesive sediment in steady-state flow

Fractal dimensions of particle populations of cohesive sediment were examined during deposition experiments in an annular flume at four conditions of steady-state flow (0.058, 0.123, 0.212 and 0.323 Pa). Light microscopy and an image analysis system were used to determine area, longest axis and perimeter of suspended solids. Four fractal dimensions ( D, D 1, D 2, D k ) were calculated from the slopes of regression lines of the relevant variables on double log plots. The fractal dimension D, which relates the projected area ( A) to the perimeter ( P) of the particle ( P∝ A D/2 ), increased from 1.25±0.005 at a shear stress of 0.058 Pa to a maximum of 1.36±0.003 at 0.121 Pa then decreased to 1.34±0.001 at 0.323 Pa. The change in D indicated that particle boundaries became more convoluted and the shape of larger particles was more irregular at higher levels of shear stress. At the highest shear stress, the observed decrease in D resulted from floc breakage due to increased particle collisions. The fractal dimension D 1, which relates the longest axis ( l) to the perimeter of the particle ( P∝ l D 1 ), increased from 1.00±0.006 at a shear stress of 0.058 Pa to a maximum of 1.25±0.003 at 0.325 Pa. The fractal dimension D 2, which relates the longest axis with the projected area of the particle ( A∝ l D 2 ), increased from 1.35±0.014 at a shear stress of 0.058 Pa to a maximum of 1.81±0.005 at 0.323 Pa. The observed increases in D 1 and D 2 indicate that particles became more elongated with increasing shear stress. Values of the fractal dimension D k , resulting from the Korcak's empirical law for particle population, decreased from 3.68±0.002 at a shear stress of 0.058 Pa to 1.33±0.001 at 0.323 Pa and indicate that the particle size distribution changed from a population of similar sized particles at low shear to larger flocculated particles at higher levels of shear. The results show that small particle clusters (micro-flocs) are the formational units of larger flocs in the water column and the stability of larger flocs is a function of the shear stress at steady state.