Off-Line Analysis of Red Blood Cell Velocity in Renal Arterioles

Vriese, An S. De; Verbeuren, Tony J.; Vallez, Marie‐Odile; Lameire, Norbert; Buyzere, Marc De; Vanhoutte, Pmgr

doi:10.1159/000025710

Cited by 41 publications

(39 citation statements)

References 10 publications

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“…The instantaneous behavior of red cells flowing through microvessels were analyzed by measuring a length of movements of RBCs during consecutive two frames (frame-by-frame method) based on high-speed cinefilms recorded under microscopes with transmitted light (18) - (20) . In recent studies, instead of high-speed microcinematography, a high-speed videomicroscopy has been used (21), (22) . The red cell velocity profiles were obtained from multiple positions of fluorescence labeled cells (platelet or RBC) or particles in a single video frame.…”

Section: Discussionmentioning

confidence: 99%

Velocity Profiles of Pulsatile Blood Flow in Arterioles with Bifurcation and Confluence in Rat Mesnetery Measured by Particle Image Velocimetry

Nakano¹,

Sugii

Minamiyama

et al. 2005

JSME Int. J., Ser. C

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Blood flow velocity profile in microvessels is essential for in vivo studies of substance exchange between blood and tissue. This paper was aimed to investigate the temporal and spatial variations in the velocity profile of red blood cell (RBC) flow in arterioles with both bifurcation and confluence in the rat mesentery, using a particle image velocimetry (PIV). The microcirculation in rat mesentery was observed under a microscopic system with a high-speed digital camera. The images of RBCs flow in microvessels were recorded simultaneously with the arterial blood pressure. Based on the high-speed video images, instantaneous velocity vectors of RBCs in arterioles with bifurcation and confluence were evaluated using a high spatial-resolution PIV algorithm. Then, the time-averaged and ensemble-averaged velocity profiles over the cross-section were calculated from the proximal through the bifurcation to the distal to the confluence. The velocity profile of RBCs showed two peaks at bifurcation and confluence, respectively. The double peaks were most marked at the apex of bifurcation, but not so much marked at the confluence. The variation of centerline velocity showed that the length of vessel under the influence of bifurcation or confluence, was approximately 1.5 times the diameter at the proximal to the apex of bifurcation, but its length was reduced significantly at the distal of confluence.

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Section: Discussionmentioning

confidence: 99%

Velocity Profiles of Pulsatile Blood Flow in Arterioles with Bifurcation and Confluence in Rat Mesnetery Measured by Particle Image Velocimetry

Nakano¹,

Sugii

Minamiyama

et al. 2005

JSME Int. J., Ser. C

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“…For erythrocyte velocity measurements, sequences were recorded with the high-speed camera at a rate of 600 fps and forwarded to the video recorder at a rate of 25 fps. The sequences were thus slowed with a factor 24, allowing analysis of the erythrocyte velocities with the lineshift-diagram method [24].…”

Section: Methodsmentioning

confidence: 99%

The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - induced diabetic rats is restored by 5-methyltetrahydrofolate

et al. 2000

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Dysfunction of the endothelium is an early and key event in the development of microvascular and macrovascular complications [1], which account for most of the morbidity and mortality of diabetes. Endothelial integrity is generally assessed by evaluating the vasodilator response of a blood vessel or a vascular bed to an endothelium-dependent agonist [2]. Endothelial cells relax the tone of the underlying vascular smooth muscle cells by releasing a number of vasodi- Diabetologia (2000) Abstract Aims/hypothesis. Endothelial dysfunction contributes to the development of diabetic vascular complications. A better understanding of the pathophysiology of endothelial dysfunction in diabetes could lead to new approaches to prevent microvascular disease. Methods. Endothelium-dependent and endotheliumindependent vasodilator responses were investigated in the renal microcirculation of streptozotocin-induced diabetic rats. We measured renal blood flow changes with an electromagnetic flow probe. In addition, the responses of the different segments of the renal microcirculation were evaluated with videomicroscopy using the hydronephrotic kidney technique. Because endothelial cells release different relaxing factors (nitric oxide, prostacyclin and an unidentified endothelium-derived hyperpolarizing factor), responses to acetylcholine were measured before and after treatment with the nitric oxide synthase inhibitor l-N G -nitroarginine methylester HCI (l-NAME) and the cyclooxygenase inhibitor indomethacin. We evaluated with the effect of 5-methyltetrahydrofolate, the active form of folate, on the responses. Results. The l-NAME-and indomethacin-resistant vasodilation to intra-renal acetylcholine was significantly reduced in the diabetic compared with control rats, suggesting impaired endothelium-derived hyperpolarizing factor-mediated vasodilation. The responses to the nitric oxide donor (Z)-1-[-2-(aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) and to the K + -channel opener pinacidil were similar in diabetics and controls, indicating intact endothelium-independent vasodilator mechanisms. The contribution of endothelium-derived hyperpolarizing factor to vasodilation induced by acetylcholine was greatest in the smallest arterioles. In diabetic rats, the response to acetylcholine was increasingly impared as vessel size decreased. Defective vasodilation in diabetic kidneys was rapidly normalized by 5-methyltetrahydrofolate. Conclusion-interpretation. Endothelium-derived hyperpolarizing factor-mediated vasodilation is impaired in the renal microcirculation of diabetic rats, in particular in the smallest arteries. Treatment with folate restores the impaired endothelial function in diabetes. [Diabetologia (2000

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“…The tissue was transilluminated by a fiberoptic using a light source (KL 1500; Schott, Wiesbaden, Germany) equipped with a 150 W halogen lamp. The resulting image was displayed on a television monitor by a TK-1281 camera (Victor Company of Japan LTD-JVC, Tokyo, Japan) or a highspeed video camera (Kodak Motioncorder Analyzer; Eastman Kodak Company, San Diego, CA) and video recorded (S-VHS Panasonic AG-7350; Panasonic, Matsushita, Japan) for offline analysis with an image analysis software program (Cap-Image; Ingenieurbüro Zeintl, Heidelberg, Germany) as previously described by De Vriese and Lameire 13 and De Vriese et al 71 The number of rolling, adhering, and extravasated leukocytes, leukocyte rolling velocity, V RBC , and VD were measured three times at each time point. VWSR was calculated as VWSR=83V RBC /D.…”

Section: Intravital Microscopymentioning

confidence: 99%

Protein-Bound Uremic Toxins Stimulate Crosstalk between Leukocytes and Vessel Wall

Pletinck

Glorieux

Schepers

et al. 2013

Journal of the American Society of Nephrology

100

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Leukocyte activation and endothelial damage both contribute to cardiovascular disease, a major cause of morbidity and mortality in CKD. Experimental in vitro data link several protein-bound uremic retention solutes to the modulation of inflammatory stimuli, including endothelium and leukocyte responses and cardiovascular damage, corroborating observational in vivo data. However, the impact of these uremic toxins on the crosstalk between endothelium and leukocytes has not been assessed. This study evaluated the effects of acute and continuous exposure to uremic levels of indoxylsulfate (IS), p-cresylsulfate (pCS), and p-cresylglucuronide (pCG) on the recruitment of circulating leukocytes in the rat peritoneal vascular bed using intravital microscopy. Superfusion with IS induced strong leukocyte adhesion, enhanced extravasation, and interrupted blood flow, whereas pCS caused a rapid increase in leukocyte rolling. Superfusion with pCS and pCG combined caused impaired blood flow and vascular leakage but did not further enhance leukocyte rolling over pCS alone. Intravenous infusion with IS confirmed the superfusion results and caused shedding of heparan sulfate, pointing to disruption of the glycocalyx as the mechanism likely mediating IS-induced flow stagnation. These results provide the first clear in vivo evidence that IS, pCS, and pCG exert proinflammatory effects that contribute to vascular damage by stimulating crosstalk between leukocytes and vessels.

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Off-Line Analysis of Red Blood Cell Velocity in Renal Arterioles

Cited by 41 publications

References 10 publications

Velocity Profiles of Pulsatile Blood Flow in Arterioles with Bifurcation and Confluence in Rat Mesnetery Measured by Particle Image Velocimetry

Velocity Profiles of Pulsatile Blood Flow in Arterioles with Bifurcation and Confluence in Rat Mesnetery Measured by Particle Image Velocimetry

The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - induced diabetic rats is restored by 5-methyltetrahydrofolate

Protein-Bound Uremic Toxins Stimulate Crosstalk between Leukocytes and Vessel Wall

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