scholarly journals Arterial wall shear rate response to reactive hyperaemia is markedly different between young and older humans

2019 ◽  
Vol 597 (16) ◽  
pp. 4151-4163
Author(s):  
Kunihiko Aizawa ◽  
Alessandro Ramalli ◽  
Sara Sbragi ◽  
Piero Tortoli ◽  
Francesco Casanova ◽  
...  
Keyword(s):  
Shear Rate ◽  
Arterial Wall ◽  
Wall Shear Rate ◽  
Reactive Hyperaemia ◽  
Wall Shear

Fluid Filtration across the Arterial Wall under Flow Conditions: Is Wall Shear Rate Another Factor Affecting Filtration Rate?a

1998 ◽  
Vol 858 (1 BIOTRANSPORT) ◽  
pp. 105-115 ◽  
Author(s):  
XIAOYAN DENG ◽  
YVES MAROIS ◽  
ROBERT GUIDOIN
Keyword(s):  
Shear Rate ◽  
Filtration Rate ◽  
Arterial Wall ◽  
Wall Shear Rate ◽  
Flow Conditions ◽  
Fluid Filtration ◽  
Wall Shear

scholarly journals Reduced thrombus formation in native blood of homozygous factor VII- deficient patients at high arterial wall shear rate

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3371-3377 ◽  
Author(s):  
RM Barstad ◽  
H Stormorken ◽  
L Orning ◽  
RW Stephens ◽  
LB Petersen ◽  
...  
Keyword(s):  
Shear Rate ◽  
Arterial Wall ◽  
Thrombus Formation ◽  
Wall Shear Rate ◽  
Factor Vii ◽  
High Shear ◽  
Shear Rates ◽  
Perfusion Chamber ◽  
Wall Shear ◽  
Shear Condition

Abstract Inhibition of thrombin formation in flowing native blood reduces thrombus formation on subendothelium, dacron, or collagen fibrils at arterial wall shear rates of 450 to 650 s-1. In the present study, we have investigated the role of low levels of factor VII (FVII) in thrombus formation on collagen fibrils at arterial wall shear rates of 650 s-1 (coronary arteries), 2,600 s-1 (mildly stenosed arteries), and 10,510 s-1 (severely stenosed arteries) in parallel-plate perfusion chambers. In the perfusion chamber with the highest wall shear rate, thrombus formation took place at the apex of an eccentric stenosis, which reduced the cross-sectional area of the blood flow channel by 80%, thus simulating thrombus formation at an atherosclerotic plaque rupture. Native blood from 21 healthy volunteers and 12 homozygous FVII- deficient patients was drawn by a pump directly from an antecubital vein over a surface of fibrillar collagen positioned in the respective perfusion chambers. The patients had FVII coagulant activities ranging from 1.3% to 4.5% and FVII antigen levels of 16% to 23% of normal. Immunoaffinity purification of the patients' FVII followed by electrophoresis (sodium dodecyl sulfate-polyacrylamide gel electrophoresis [SDS-PAGE]) and immunoblotting showed a protein with similar molecular mass as normal FVII. In the perfusion studies, a reduction in thrombus volume of 54% of normal (P < .007) at 10,510 s-1 was observed. The deposition of fibrin on the thrombogenic surface and the plasma level of fibrinopeptide A (FPA) in blood samples collected distal to the perfusion chamber were concomitantly reduced (P < .002 and P < .04, respectively). The plasma FPA level was also reduced at 2,600 s-1 (P < .04), but not at 650 s-1. However, at the lower shear conditions, the thrombus volume and the fibrin deposition were within the ranges observed in normal blood. The platelet-collagen adhesion was not affected at any of the three shear conditions. Thus, low plasma levels of FVII result in significantly less formation of thrombin and fibrin in and around growing platelet masses at high shear condition. This may weaken the thrombus stability and reduce platelet recruitment, thereby lowering thrombus volume. In support of this theory, one patient with afibrinogenemia had an 83% reduction in thrombus volume at this high shear condition.

scholarly journals Reduced thrombus formation in native blood of homozygous factor VII- deficient patients at high arterial wall shear rate

Blood ◽  
1994 ◽  
Vol 84 (10) ◽  
pp. 3371-3377
Author(s):  
RM Barstad ◽  
H Stormorken ◽  
L Orning ◽  
RW Stephens ◽  
LB Petersen ◽  
...  
Keyword(s):  
Shear Rate ◽  
Arterial Wall ◽  
Thrombus Formation ◽  
Wall Shear Rate ◽  
Factor Vii ◽  
High Shear ◽  
Shear Rates ◽  
Perfusion Chamber ◽  
Wall Shear ◽  
Shear Condition

Inhibition of thrombin formation in flowing native blood reduces thrombus formation on subendothelium, dacron, or collagen fibrils at arterial wall shear rates of 450 to 650 s-1. In the present study, we have investigated the role of low levels of factor VII (FVII) in thrombus formation on collagen fibrils at arterial wall shear rates of 650 s-1 (coronary arteries), 2,600 s-1 (mildly stenosed arteries), and 10,510 s-1 (severely stenosed arteries) in parallel-plate perfusion chambers. In the perfusion chamber with the highest wall shear rate, thrombus formation took place at the apex of an eccentric stenosis, which reduced the cross-sectional area of the blood flow channel by 80%, thus simulating thrombus formation at an atherosclerotic plaque rupture. Native blood from 21 healthy volunteers and 12 homozygous FVII- deficient patients was drawn by a pump directly from an antecubital vein over a surface of fibrillar collagen positioned in the respective perfusion chambers. The patients had FVII coagulant activities ranging from 1.3% to 4.5% and FVII antigen levels of 16% to 23% of normal. Immunoaffinity purification of the patients' FVII followed by electrophoresis (sodium dodecyl sulfate-polyacrylamide gel electrophoresis [SDS-PAGE]) and immunoblotting showed a protein with similar molecular mass as normal FVII. In the perfusion studies, a reduction in thrombus volume of 54% of normal (P < .007) at 10,510 s-1 was observed. The deposition of fibrin on the thrombogenic surface and the plasma level of fibrinopeptide A (FPA) in blood samples collected distal to the perfusion chamber were concomitantly reduced (P < .002 and P < .04, respectively). The plasma FPA level was also reduced at 2,600 s-1 (P < .04), but not at 650 s-1. However, at the lower shear conditions, the thrombus volume and the fibrin deposition were within the ranges observed in normal blood. The platelet-collagen adhesion was not affected at any of the three shear conditions. Thus, low plasma levels of FVII result in significantly less formation of thrombin and fibrin in and around growing platelet masses at high shear condition. This may weaken the thrombus stability and reduce platelet recruitment, thereby lowering thrombus volume. In support of this theory, one patient with afibrinogenemia had an 83% reduction in thrombus volume at this high shear condition.

8.10 BRACHIAL ARTERY FLOW-MEDIATED DILATATION: DIFFERENT PATTERNS OF WALL SHEAR RATE INCREASE DURING REACTIVE HYPERAEMIA

2016 ◽  
Vol 16 (C) ◽  
pp. 67
Author(s):  
Kunihiko Aizawa ◽  
Sara Sbragi ◽  
Alessandro Ramalli ◽  
Piero Tortoli ◽  
Francesco Casanova ◽  
...  
Keyword(s):  
Shear Rate ◽  
Brachial Artery ◽  
Rate Increase ◽  
Wall Shear Rate ◽  
Reactive Hyperaemia ◽  
Flow Mediated Dilatation ◽  
Wall Shear ◽  
Artery Flow

scholarly journals Brachial artery vasodilatory response and wall shear rate determined by multigate Doppler in a healthy young cohort

2018 ◽  
Vol 124 (1) ◽  
pp. 150-159 ◽  
Author(s):  
Kunihiko Aizawa ◽  
Sara Sbragi ◽  
Alessandro Ramalli ◽  
Piero Tortoli ◽  
Francesco Casanova ◽  
...  
Keyword(s):  
Shear Rate ◽  
Brachial Artery ◽  
Arterial Wall ◽  
Reactive Hyperemia ◽  
Wall Shear Rate ◽  
Young Cohort ◽  
Flow Mediated Dilation ◽  
Detailed Measurement ◽  
Vascular Physiology ◽  
Wall Shear

Wall shear rate (WSR) is an important stimulus for the brachial artery flow-mediated dilation (FMD) response. However, WSR estimation near the arterial wall by conventional Doppler is inherently difficult. To overcome this limitation, we utilized multigate Doppler to accurately determine the WSR stimulus near the vessel wall simultaneously with the FMD response using an integrated FMD system [Ultrasound Advanced Open Platform (ULA-OP)]. Using the system, we aimed to perform a detailed analysis of WSR-FMD response and establish novel WSR parameters in a healthy young population. Data from 33 young healthy individuals (27.5 ± 4.9 yr, 19 females) were analyzed. FMD was assessed with reactive hyperemia using ULA-OP. All acquired raw data were postprocessed using custom-designed software to obtain WSR and diameter parameters. The acquired velocity data revealed that nonparabolic flow profiles within the cardiac cycle and under different flow states, with heterogeneity between participants. We also identified seven WSR magnitude and four WSR time-course parameters. Among them, WSR area under the curve until its return to baseline was the strongest predictor of the absolute ( R2 = 0.25) and percent ( R2 = 0.31) diameter changes in response to reactive hyperemia. For the first time, we identified mono- and biphasic WSR stimulus patterns within our cohort that produced different magnitudes of FMD response [absolute diameter change: 0.24 ± 0.10 mm (monophasic) vs. 0.17 ± 0.09 mm (biphasic), P < 0.05]. We concluded that accurate and detailed measurement of the WSR stimulus is important to comprehensively understand the FMD response and that this advance in current FMD technology could be important to better understand vascular physiology and pathology. NEW & NOTEWORTHY An estimation of wall shear rate (WSR) near the arterial wall by conventional Doppler ultrasound is inherently difficult. Using a recently developed integrated flow-mediated dilation ultrasound system, we were able to accurately estimate WSR near the wall and identified a number of novel WSR variables that may prove to be useful in the measurement of endothelial function, an important biomarker of vascular physiology and disease.

Atheroma and arterial wall shear - Observation, correlation and proposal of a shear dependent mass transfer mechanism for atherogenesis

1971 ◽  
Vol 177 (1046) ◽  
pp. 109-133 ◽  
Keyword(s):  
Shear Rate ◽  
Mass Transport ◽  
Concentration Gradient ◽  
Arterial Wall ◽  
Wall Shear Rate ◽  
Main Stream ◽  
High Shear ◽  
Wall Shear ◽  
Dependent Mass ◽  
Low Shear

On the basis of various observations, we argue that there is spatial variation of the time averaged wall shear rate in arteries, both overall and locally. From our own observations, and those of others, we show that the distribution of early atheroma in man is coincident with those regions in which arterial wall shear rate is expected to be relatively low, while the development of lesions is inhibited or retarded in those regions in which wall shear rate is expected to be relatively high. Such a correlation is inconsistent with a proposal, made by several workers, that there is a causative relation between arterial blood mechanics and the development of atheroma, i. e. that atheroma is associated with wall damage due to the motion of blood. Instead it immediately suggests that the process is associated with shear dependent mass transport phenomena. It has been demonstrated by others that mass transport, in the inner part of the arterial wall, is dominantly to and from blood flowing within the lumen. We review theory relevant to diffusional mass transport across such a sheared interface, and examine available experimental evidence, relating to normally occurring (quasi-steady state) and experimentally induced (transient-type) atheroma, as well as the distribution of cholesterol in arteries. These results are considered in the light of simple theoretical schemes which we develop for the movement of cholesterol, in particular, although the arguments may also be relevant to other diffusing species. Shear enhances mass transport by means of a steepening effect on the concentration gradient, thus diffusion of material from a wall is promoted when material which has already diffused is swept rapidly away, so that the concentration gradient leading to further diffusion remains steep. However, the influence of shear on the diffusion of a species, say, from just within the wall of an artery to fluid in the main stream, depends upon the relative resistances to its diffusion from within the wall to surface fluid (wall phase) and from surface fluid to fluid in the main stream (blood phase); diffusion is not appreciably shear dependent if the latter resistance is small compared with the former. Assuming simplified flow conditions and that as suggested by others cholesterol is transported in blood in association with plasma protein, we can estimate resistance for diffusion of this species in the blood phase, for different stations in the arterial system. However, we possess no definite comparable information for the wall phase; we conjecture that this resistance is relatively small, and assume shear dependence of diffusional transport of cholesterol between arterial walls and intraluminal blood. We find that a net flux of cholesterol from blood to wall, as has been suggested by others, cannot account, in terms of the proposed schemes, for the observed normally occurring (quasi-steady state) distribution of atheromatous lesions in man and in animals; mass transport is inhibited in low shear regions by the thick diffusional boundary layer. Instead it appears that cholesterol, which has been shown by others to be synthesized in arterial walls, accumulates in low shear regions because its local diffusional efflux from wall to blood is inhibited by the reduced concentration gradient. Given suitable values for relevant parameters, the theoretical schemes are also able to account for adequacy of supply of precursor to the wall for cholesterol synthesis, for the preferential occurrence that we now recognize of lesions in high shear regions in response to sudden natural or experimental elevation of blood cholesterol, and for the responses to administration of labelled cholesterol (transient type phenomena); it appears therefore possible, in terms of these schemes, to unify naturally occurring and experimentally induced atheroma. It is reported by others that platelets are associated only with advanced lesions; the correlation of naturally occurring atheroma with low shear regions, and transient type lesions with high shear regions, with the fluid mechanics being unaltered in the two situations, provides no support for the implication of platelets in the development of early atheroma. It appears that wall shear rate may be a major controlling factor in the development of atheroma, i.e. that high shear, such as is associated for example with increased cardiac output in exercise, will retard progression of the process. Its progression will also be retarded by any means which reduces the accumulation of atheromatous material, by influencing its rate of net production or diffusion.

scholarly journals Importance of Primary Capture and L-Selectin–Dependent Secondary Capture in Leukocyte Accumulation in Inflammation and Atherosclerosis in Vivo

2001 ◽  
Vol 194 (2) ◽  
pp. 205-218 ◽  
Author(s):  
Einar E. Eriksson ◽  
Xun Xie ◽  
Joachim Werr ◽  
Peter Thoren ◽  
Lennart Lindbom
Keyword(s):  
Shear Rate ◽  
Leukocyte Recruitment ◽  
Wall Shear Rate ◽  
Free Flow ◽  
Initial Contact ◽  
Atherosclerotic Lesions ◽  
Leukocyte Accumulation ◽  
Wall Shear ◽  
Rolling Leukocytes

In the multistep process of leukocyte extravasation, the mechanisms by which leukocytes establish the initial contact with the endothelium are unclear. In parallel, there is a controversy regarding the role for L-selectin in leukocyte recruitment. Here, using intravital microscopy in the mouse, we investigated leukocyte capture from the free flow directly to the endothelium (primary capture), and capture mediated through interactions with rolling leukocytes (secondary capture) in venules, in cytokine-stimulated arterial vessels, and on atherosclerotic lesions in the aorta. Capture was more prominent in arterial vessels compared with venules. In venules, the incidence of capture increased with increasing vessel diameter and wall shear rate. Secondary capture required a minimum rolling leukocyte flux and contributed by ∼20–50% of total capture in all studied vessel types. In arteries, secondary capture induced formation of clusters and strings of rolling leukocytes. Function inhibition of L-selectin blocked secondary capture and thereby decreased the flux of rolling leukocytes in arterial vessels and in large (&gt;45 μm in diameter), but not small (&lt;45 μm), venules. These findings demonstrate the importance of leukocyte capture from the free flow in vivo. The different impact of blockage of secondary capture in venules of distinct diameter range, rolling flux, and wall shear rate provides explanations for the controversy regarding the role of L-selectin in various situations of leukocyte recruitment. What is more, secondary capture occurs on atherosclerotic lesions, a fact that provides the first evidence for roles of L-selectin in leukocyte accumulation in atherogenesis.

scholarly journals Influence of arterial damage and wall shear rate on platelet deposition. Ex vivo study in a swine model.

1986 ◽  
Vol 6 (3) ◽  
pp. 312-320 ◽  
Author(s):  
L Badimon ◽  
J J Badimon ◽  
A Galvez ◽  
J H Chesebro ◽  
V Fuster
Keyword(s):  
Shear Rate ◽  
Ex Vivo ◽  
Wall Shear Rate ◽  
Swine Model ◽  
Platelet Deposition ◽  
Wall Shear ◽  
Arterial Damage ◽  
Ex Vivo Study

Factors Associated with Impaired Arterial Adaptation to Chronically High Wall Shear Rate in the Feeding Artery of PTFE Grafts

2008 ◽  
Vol 28 (5) ◽  
pp. 847-852 ◽  
Author(s):  
Vladimir Tuka ◽  
Marcela Slavikova ◽  
Zdislava Kasalova ◽  
Jan Malik
Keyword(s):  
Shear Rate ◽  
Wall Shear Rate ◽  
Feeding Artery ◽  
Factors Associated ◽  
Wall Shear

Viscous boundary layers in reversing flow

1976 ◽  
Vol 74 (1) ◽  
pp. 59-79 ◽  
Author(s):  
T. J. Pedley
Keyword(s):  
Boundary Layer ◽  
Shear Rate ◽  
Leading Edge ◽  
Wall Shear Rate ◽  
Viscous Boundary Layer ◽  
Large Molecules ◽  
Displacement Thickness ◽  
The Mean ◽  
Wall Shear ◽  
Viscous Boundary

The viscous boundary layer on a finite flat plate in a stream which reverses its direction once (at t = 0) is analysed using an improved version of the approximate method described earlier (Pedley 1975). Long before reversal (t < −t1), the flow at a point on the plate will be quasi-steady; long after reversal (t > t2), the flow will again be quasi-steady, but with the leading edge at the other end of the plate. In between (−t1 < t < t2) the flow is governed approximately by the diffusion equation, and we choose a simple solution of that equation which ensures that the displacement thickness of the boundary layer remains constant at t = −t1. The results of the theory, in the form of the wall shear rate at a point as a function of time, are given both for a uniformly decelerating stream, and for a sinusoidally oscillating stream which reverses its direction twice every cycle. The theory is further modified to cover streams which do not reverse, but for which the quasi-steady solution breaks down because the velocity becomes very small. The analysis is also applied to predict the wall shear rate at the entrance to a straight pipe when the core velocity varies with time as in a dog's aorta. The results show positive and negative peak values of shear very much larger than the mean. They suggest that, if wall shear is implicated in the generation of atherosclerosis because it alters the permeability of the wall to large molecules, then an appropriate index of wall shear at a point is more likely to be the r.m.s. value than the mean.

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