In Vitro Evaluation of Flow Divertors in an Elastase-Induced Saccular Aneurysm Model in Rabbit

2007 ◽  
Vol 129 (6) ◽  
pp. 863-872 ◽  
Author(s):  
Jaehoon Seong ◽  
Ajay K. Wakhloo ◽  
Baruch B. Lieber
Keyword(s):  
Shear Rate ◽  
Kinetic Energy ◽  
Wall Shear Rate ◽  
Endovascular Coiling ◽  
Aneurysm Neck ◽  
The Mean ◽  
Wall Shear ◽  
Aneurysm Model

Endovascular coiling is an acceptable treatment of intracranial aneurysms, yet long term follow-ups suggest that endovascular coiling fails to achieve complete aneurysm occlusions particularly in wide-neck and giant aneurysms. Placing of a stentlike device across the aneurysm neck may be sufficient to occlude the aneurysm by promoting intra-aneurysmal thrombosis; however, conclusive evidence of its efficacy is still lacking. In this study, we investigate in vitro the efficacy of custom designed flow divertors that will be subsequently implanted in a large cohort of animals. The aim of this study is to provide a detailed database against which in vivo results can be analyzed. Six custom designed flow divertors were fabricated and tested in vitro. The design matrix included three different porosities (75%, 70%, and 65%). For each porosity, there were two divertors with one having a nominal pore density double than that of the other. To quantify efficacy, the divertors were implanted in a compliant elastomeric model of an elastase-induced aneurysm model in rabbit and intra-aneurysmal flow changes were evaluated by particle image velocimetry (PIV). PIV results indicate a marked reduction in intra-aneurysmal flow activity after divertor implantation in the innominate artery across the aneurysm neck. The mean hydrodynamic circulation after divertor implantation was reduced to 14% or less of the mean circulation in the control and the mean intra-aneurysmal kinetic energy was reduced to 29% or less of its value in the control. The intra-aneurysmal wall shear rate in this model is low and implantation of the flow divertor did not change the wall shear rate magnitude appreciably. This in vitro experiment evaluates the characteristics of local flow phenomena such as hydrodynamic circulation, kinetic energy, wall shear rate, perforator flow, and changes of these parameters as a result of implantation of stentlike flow divertors in an elastomeric replica of elastase-induced saccular aneurysm model in rabbit. These initial findings offer a database for evaluation of in vivo implantations of such devices in the animal model and help in further development of cerebral aneurysm bypass devices.

Design, fabrication, and in vitro evaluation of an in vivo ultrasonic Doppler wall shear rate measuring device

1995 ◽  
Vol 42 (5) ◽  
pp. 433-441 ◽  
Author(s):  
R.S. Keynton ◽  
R.E. Nemer ◽  
Q.Y. Neifert ◽  
R.S. Fatemi ◽  
S.E. Rittgers
Keyword(s):  
Shear Rate ◽  
Wall Shear Rate ◽  
Measuring Device ◽  
In Vitro Evaluation ◽  
Wall Shear

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 (>45 μm in diameter), but not small (<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.

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.

scholarly journals In Vivo Vascular Wall Shear Rate and Circumferential Strain of Renal Disease Patients

2013 ◽  
Vol 39 (2) ◽  
pp. 241-252 ◽  
Author(s):  
Dae Woo Park ◽  
Grant H. Kruger ◽  
Jonathan M. Rubin ◽  
James Hamilton ◽  
Paul Gottschalk ◽  
...  
Keyword(s):  
Shear Rate ◽  
Renal Disease ◽  
Circumferential Strain ◽  
Vascular Wall ◽  
Wall Shear Rate ◽  
Wall Shear

Therapeutic Amelioration of Vaso-Occlusion and Blood Flow Impairment in Transgenic Sickle Mice By the Antioxidant Flavonoid Quercetin

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4054-4054
Author(s):  
Sangeetha Thangaswamy ◽  
Henny H Billett ◽  
Craig A. Branch ◽  
Sandra M. Suzuka ◽  
Seetharama A Acharya
Keyword(s):  
Blood Flow ◽  
Shear Rate ◽  
Leukocyte Adhesion ◽  
Flow Direction ◽  
Radical Scavenging ◽  
Wall Shear Rate ◽  
Cremaster Muscle ◽  
Wild Type ◽  
Wall Shear

Abstract Sickle cell disease (SCD) is characterized by painful vaso-occlusive crises, which are, at least in part, due to an interaction of the sickle RBC (sRBC) with the vascular endothelium. Abnormal red blood cells (RBCs) impair blood flow and contribute to microcirculatory complications. Oxidative stress and/or oxidants generated via hemoglobin S (HbS) auto-oxidation play a vital role in the vaso-occlusive event in SCD. Antioxidant therapy mediated free radical scavenging and attenuation of oxidative stress may reduce red cell sickling and be beneficial for SCD. Several studies have described an antioxidant effect of flavonoids on the attenuation of free radical mediated biological membrane damage and the consumption of flavonoids reduces the prevalence of vascular diseases. Among flavonoids, quercetin (QUE) pentahydroxy flavone is the major representative. In vitro, QUE is a strong antioxidant with alkoxyl and peroxy radical scavenging ability. Due to the high susceptibility of sickle RBC to oxidation, QUE could be a useful therapy for SCD. Based on this concept, we examined the potential effect of QUE to improve microvascular function in a murine model of SCD. Methods: To confirm the protective effect of quercetin in vivo, we used Berkeley (Berk) sickle transgenic mice which express exclusively human α- and βS-globins with low levels of γ-globin (∼ 3-5%) generated by Paszty et al 1997. C57BL /6J were used as control wild type. We injected a single dose of QUE at different concentrations (50, 100, 200mg/kg body weight) intraperitoneally under normoxic conditions. Three hours after QUE administration, in vivo intra-vital microscopic observation of post-capillary venules in cremaster muscle was performed. The luminal diameters of the venules (∼ 20-40 µm diameter), centerline red blood cell velocity (Vrbc), adherent, emigrated and rolling leukocytes were measured by the technique described by Kaul et al 2004. Wall shear rate was calculated by Lipowsky et al, 1980. Results: QUE treatment restored blood flow, as evidenced by complete disappearance of vaso-occlusion in the postcapillary venules of Berk mice (Figure 1). However, no significant differences in venular diameter were noted with QUE treatment at any of the dose levels tested (50, 100, 200mg/kg) when compared to untreated Berk and wild type mice. But, when compared to untreated Berk mice, a significant increase in the RBC velocity was demonstrated in a dose dependent fashion (treated: 1.74 ±1.3 mm/sec, 3.02± 1.2 mm/sec, 3.4±0.90 mm/sec for 50, 100, 200 mg/kg dosing respectively vs. untreated 1.01± 1.05mm/sec, p<0.05). A dose of 200 mg level completely neutralized the vaso-occlusion. Increases in wall shear rate (650.01± 252.05 s-1 vs. 180.12± 165.02 s-1, p<6.03x10-6) was also observed in QUE treated vs. untreated Berk. This improvement of blood flow in the postcapillary venules correlated well with observed decreases in leukocyte adhesion (Figure 2A) and leukocyte emigration (Figure 2B) in QUE treated Berk mice (for doses 50, 100, and 200mg/kg) when compared to untreated Berk mice. Leukocyte rolling was also decreased for doses 100 and 200mg/kg (p<0.007, p<0.0002 respectively) after treatment with QUE when compared to untreated Berk and wild type. Figure 1: Representative images showing postcapillary venules in the cremaster muscle microcirculation of Berk mice compared to QUE treated and wild type. Black arrows indicate leukocytes and white arrows indicate the blood flow direction. Figure 1:. Representative images showing postcapillary venules in the cremaster muscle microcirculation of Berk mice compared to QUE treated and wild type. Black arrows indicate leukocytes and white arrows indicate the blood flow direction. Figure 2: Leukocyte adhesion (2A) and emigration (2B) in QUE treated Berk mice at 50, 100 and 200mg/kg doses compared to untreated Berk and wild type. Figure 2:. Leukocyte adhesion (2A) and emigration (2B) in QUE treated Berk mice at 50, 100 and 200mg/kg doses compared to untreated Berk and wild type. Figure 3 Figure 3. Conclusion: We observed an improvement in RBC velocity and wall shear rate, as well as a complete attenuation of leukocyte adhesion, rolling and emigration at the highest dose of QUE treated transgenic sickle Berk mice. We suggest that these effects may be due to a decreased sickle RBC interaction with the vascular bed. Our present data provide a strong basis for the therapeutic application of flavonoids in SCD. Further studies are needed to better understand the mechanism of action in vivo for therapeutic effect in SCD. Disclosures Thangaswamy: AMI Life Sciences Private Ltd: Drug supplied Other. Billett:Selexys Pharmaceuticals: Research Funding.

scholarly journals Feasibility of in vivo measurement of carotid wall shear rate using spiral fourier velocity encoded MRI

2010 ◽  
Vol 63 (6) ◽  
pp. 1537-1547 ◽  
Author(s):  
Joao L. A. Carvalho ◽  
Jon-Fredrik Nielsen ◽  
Krishna S. Nayak
Keyword(s):  
Shear Rate ◽  
Wall Shear Rate ◽  
In Vivo Measurement ◽  
Carotid Wall ◽  
Wall Shear

Wall shear rate in arterioles in vivo: least estimates from platelet velocity profiles

1988 ◽  
Vol 254 (6) ◽  
pp. H1059-H1064 ◽  
Author(s):  
G. J. Tangelder ◽  
D. W. Slaaf ◽  
T. Arts ◽  
R. S. Reneman
Keyword(s):  
Shear Rate ◽  
Velocity Gradient ◽  
Velocity Profiles ◽  
Wall Shear Rate ◽  
Mean Velocity ◽  
Shear Rates ◽  
Spatial Differences ◽  
Data Points ◽  
Wall Shear

Velocity profiles, as determined in vivo in rabbit mesenteric arterioles with fluorescently labeled platelets as natural flow markers, were used to calculate least estimates of the actual wall shear rate in these microvessels (17–32 micron diam). The fit of the velocity data points described the profile as close to the wall as 0.5 micron. To satisfy the no-slip condition, a thin layer of fluid with a steep velocity gradient near the wall was assumed. Least estimates of wall shear rate, as calculated from the fitted platelet-velocity profiles and using the mean velocity gradient in this layer of fluid, ranged from 472 to 4,712 s-1 with a median value of 1,700 s-1. Red blood cell center-line velocities varied between 1.3 and 14.4 mm/s (median 3.4). The wall shear rates were at least 1.46–3.94 (median 2.12) times higher than expected on the basis of a parabolic velocity distribution but with the same volume flow in the vessel. Considerable spatial differences in wall shear rate might exist even within a short segment of a vessel.

Wall Shear Rate Distribution in an Abdominal Aortic Bifurcation Model: Effects of Vessel Compliance and Phase Angle Between Pressure and Flow Waveforms

1997 ◽  
Vol 119 (3) ◽  
pp. 333-342 ◽  
Author(s):  
C. S. Lee ◽  
J. M. Tarbell
Keyword(s):  
Shear Rate ◽  
Phase Angle ◽  
Wall Motion ◽  
Outer Wall ◽  
Wall Shear Rate ◽  
Rate Distribution ◽  
Abdominal Aortic ◽  
The Mean ◽  
Wall Shear ◽  
Low Shear

The goal of this study was to determine how vessel compliance (wall motion) and the phase angle between pressure and flow waves (impedance phase angle) affect the wall shear rate distribution in an atherogenic bifurcation geometry under sinusoidal flow conditions. Both rigid and elastic models replicating the human abdominal aortic bifurcation were fabricated and the wall shear rate distribution in the median plane of the bifurcation was determined using the photochromic flow visualization method. In the elastic model, three phase angle conditions were simulated (+12, −17, −61 deg), and the results compared with those obtained in a similar rigid model. The study indicates a very low (magnitude close to zero) and oscillatory wall shear rate zone within 1.5 cm distal to the curvature site on the outer (lateral) wall. In this low shear rate zone, unsteadiness (pulsatility) of the flow greatly reduces the mean (time-averaged) wall shear rate level. Vessel wall motion reduces the wall shear rate amplitude (time-varying component) up to 46 percent depending on the location and phase angle in the model. The mean wall shear rate is less influenced by the wall motion, but is reduced significantly in the low shear region (within 1.5 cm distal to the curvature site on the outer wall), thus rendering the wall shear rate waveform more oscillatory and making the site appear more atherogenic. The effect of the phase angle is most noteworthy on the inner wall close to the flow divider tip where the mean and amplitude of wall shear rate are 31 and 23 percent lower, respectively, at the phase angle of −17 deg than at −61 deg. However, the characteristics of the wall shear rate distribution in the low shear rate zone on the outer wall that are believed to influence localization of atherosclerotic disease, such as the mean wall shear rate level, oscillation in the wall shear rate waveform, and the length of the low and oscillatory wall shear rate zone, are similar for the three phase angles considered. The study also showed a large spatial variation of the phase angle between the wall shear stress waveform and the circumferential stress waveform (hoop stress due to radial artery expansion in response to pressure variations) near the bifurcation (up to 70 deg). The two stresses became more out of phase in the low mean shear rate zone on the outer wall (wall shear stress wave leading hoop stress wave as much as 125 deg at the pressure-flow phase angle of −61 deg) and were significantly influenced by the impedance phase angle.

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