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

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.

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.

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

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.

scholarly journals Carotid Wall Shear Rate as a Marker of Systemic Atherosclerosis and Atherosclerotic Cardiovascular Disease

Kardiologiia ◽  
2019 ◽  
Vol 59 (5) ◽  
pp. 45-52
Author(s):  
V. V. Genkel ◽  
I. I. Shaposhnik
Keyword(s):  
Cardiovascular Disease ◽  
Shear Rate ◽  
Ankle Brachial Index ◽  
Density Lipoprotein ◽  
Intima Media Thickness ◽  
Wall Shear Rate ◽  
Atherosclerotic Cardiovascular Disease ◽  
Peripheral Arteries ◽  
Carotid Wall ◽  
Wall Shear

Aim: to assess possibility of the use of carotid wall shear rate (WSR) as a marker of systemic atherosclerosis and atherosclerotic cardiovascular disease (ASCVD).Materials and methods. We included into this study 200 patients with different cardiovascular risk (142 patients already had one or more ASCVD). All patients underwent ultrasound scanning of carotid and lower limb arteries with measurement of the ankle-brachial index. Carotid WSR was determined during ultrasonic scanning of carotid arteries in accordance with the Hagen-Poiseuille law.Results. Mean WSR value in this cohort of patients was 434±139 s–1. Based on the results of the ROCanalysis, it was found that WSR below the threshold value of 300 s–1 allowed to predict the presence of ASCVD with sensitivity of 97.1 % and specificity of 84.6 %. WSR <300 s–1 was associated with relative risk (RR) of ASCVD presence 11.2 (95 % CI 1.26–99.3, p=0.03), adjusted for factors such as sex, age, smoking, obesity, hypertension, estimated glomerular filtration rate (eGFR), low density lipoprotein cholesterol, and high sensitivity C-reactive protein, carotid intima-media thickness. The model which included carotid WSR, as well as factors such as the presence of type 2 diabetes, obesity, sex, age, eGFR, allowed to diagnose combined atherosclerotic lesions of peripheral arteries with a sensitivity of 73.1 % and a specificity of 90.3 %.Conclusion. Evaluation of the carotid WSR allows to diagnose with satisfactory sensitivity and specificity the presence of combined atherosclerosis of peripheral arteries and ASCVD. 

scholarly journals Common Carotid Wall Shear Stress and Carotid Atherosclerosis in End-Stage Renal Disease Patients

2012 ◽  
pp. 355-361 ◽  
Author(s):  
J. MALÍK ◽  
J. KUDLIČKA ◽  
V. TUKA ◽  
E. CHYTILOVÁ ◽  
J. ADAMEC ◽  
...  
Keyword(s):  
Shear Stress ◽  
Shear Rate ◽  
Wall Shear Stress ◽  
Carotid Bifurcation ◽  
Wall Shear Rate ◽  
Carotid Wall ◽  
Wall Shear ◽  
End Stage ◽  
Common Carotid Arteries ◽  
Esrd Patients

Decrease of arterial wall shear stress (WSS) is associated with higher probability of atherosclerotic plaque development in many disease conditions. End-stage renal diseases (ESRD) patients suffer from vascular disease frequently, but its nature differs from general population. This study was aimed at proving an association between common carotid wall shear stress and the presence of carotid bifurcation plaques in a group of ESRD patients. ESRD subjects, planned for the creation of a dialysis access and therapy were included. Wall shear rate (WSR) was used as a surrogate of WSS and was analyzed in the common carotid arteries by duplex ultrasonography. Intima media thickness (IMT) was measured at the same site. The presence/absence of carotid bifurcation plaques was recorded. The endothelial function was estimated by the levels of von Willebrand factor (vWf). 35 ESRD patients were included (19 females, 17 diabetics). Atherosclerotic plaque was present in 53 % of bifurcations. Wall shear rate was lower in arteries with plaques (349±148 vs. 506±206 s-1, p=0.005) and was directly related to the height of IMT and inversely to the activity of vWf (r= –0.65, p=0.016). Lower wall shear rate in the common carotid arteries is linked to the endothelial dysfunction and to the presence of atherosclerotic plaques in carotid bifurcations in ESRD subjects. Faster arterial dilatation may facilitate this process in ESRD subjects.

scholarly journals A Fluid Dynamics Study in a 50 cc Pulsatile Ventricular Assist Device: Influence of Heart Rate Variability

2011 ◽  
Vol 133 (10) ◽  
Author(s):  
Jason C. Nanna ◽  
Michael A. Navitsky ◽  
Stephen R. Topper ◽  
Steven Deutsch ◽  
Keefe B. Manning
Keyword(s):  
Heart Rate ◽  
Shear Rate ◽  
Data Collection ◽  
Fluid Mechanics ◽  
Wall Shear Rate ◽  
Ventricular Assist ◽  
Shear Rates ◽  
Penn State ◽  
Wall Shear

Although left ventricular assist devices (LVADs) have had success in supporting severe heart failure patients, thrombus formation within these devices still limits their long term use. Research has shown that thrombosis in the Penn State pulsatile LVAD, on a polyurethane blood sac, is largely a function of the underlying fluid mechanics and may be correlated to wall shear rates below 500 s−1. Given the large range of heart rate and systolic durations employed, in vivo it is useful to study the fluid mechanics of pulsatile LVADs under these conditions. Particle image velocimetry (PIV) was used to capture planar flow in the pump body of a Penn State 50 cubic centimeters (cc) LVAD for heart rates of 75–150 bpm and respective systolic durations of 38–50%. Shear rates were calculated along the lower device wall with attention given to the uncertainty of the shear rate measurement as a function of pixel magnification. Spatial and temporal shear rate changes associated with data collection frequency were also investigated. The accuracy of the shear rate calculation improved by approximately 40% as the resolution increased from 35 to 12 μm/pixel. In addition, data collection in 10 ms, rather than 50 ms, intervals was found to be preferable. Increasing heart rate and systolic duration showed little change in wall shear rate patterns, with wall shear rate magnitude scaling by approximately the kinematic viscosity divided by the square of the average inlet velocity, which is essentially half the friction coefficient. Changes in in vivo operating conditions strongly influence wall shear rates within our device, and likely play a significant role in thrombus deposition. Refinement of PIV techniques at higher magnifications can be useful in moving towards better prediction of thrombosis in LVADs.

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