Concentration and Velocity Profiles of Blood Cells in the Microcirculation

Reneman, Robert S.; Woldhuis, B.; Egbrink, Mirjam G.A. oude; Slaaf, Dick W.; Tangelder, Geert Jan

doi:10.1007/978-1-4757-4421-7_3

Cited by 37 publications

(31 citation statements)

References 11 publications

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“…Centerline velocities were converted to mean blood flow velocities by multiplying with an empirical factor of 0.625 (17). Wall shear rates ( ␥ w ) were estimated as 2.12 (8V b /d), where V b is the mean blood flow velocity, d is the diameter of the vessel, and 2.12 is a median empirical correction factor obtained from actual velocity profiles measured in microvessels in vivo (18). Microvessel diameters, lengths, and rolling leukocyte velocities were measured using a digital image processing system (16).…”

Section: Methodsmentioning

confidence: 99%

Transit time of leukocytes rolling through venules controls cytokine-induced inflammatory cell recruitment in vivo.

Jung¹,

Norman²,

Scharffetter‐Kochanek³

et al. 1998

J. Clin. Invest.

245

214

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Leukocyte recruitment requires leukocyte rolling, activation, firm adhesion, and transmigration. Injection of the proinflammatory cytokine TNF-␣ induces expression of E-selectin, interleukin-8, and other adhesion molecules and chemoattractants on the endothelial surface. TNF-␣ -treated CD18 null mouse cremaster muscle venules show increased leukocyte rolling velocity and reduced leukocyte recruitment efficiency. Leukocyte recruitment in CD18 null but not wild-type mice is significantly blocked by an mAb to E-selectin. To understand this overlap between adhesion events previously considered separate, we introduce a quantitative analysis of the efficiency of induction of rolling, conversion of rolling to adhesion, and of adhesion to transmigration. We find that CD18 and E-selectin cooperate to control the time a leukocyte needs to roll through an inflamed area and to convert rolling to firm adhesion. Leukocyte rolling time, defined as the time it takes for a rolling leukocyte to pass through a defined length of a vessel segment, emerges as a unifying parameter determining the efficiency of inducing firm adhesion, which is a rate-limiting step controlling leukocyte recruitment in inflammation. We conclude that leukocytes integrate chemoattractant signals while rolling along the endothelial surface until they reach a critical level of activation and become firmly adherent.

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Section: Methodsmentioning

confidence: 99%

Transit time of leukocytes rolling through venules controls cytokine-induced inflammatory cell recruitment in vivo.

Jung¹,

Norman²,

Scharffetter‐Kochanek³

et al. 1998

J. Clin. Invest.

245

214

View full text Add to dashboard Cite

show abstract

“…Centerline venular RBC velocities were measured using a dual photodiode (26) and converted to mean blood flow velocities by multiplying by an empirical factor of 0.625 (27). Shear rates (␥ w ) were determined as: ␥ w ϭ 2.12(8V b )/d, where V b is the mean blood velocity, d is the vessel diameter, and 2.12 is a correction factor for the shape of the velocity profile (28).…”

Section: Intravital Microscopymentioning

confidence: 99%

Delayed Onset of Inflammation in Protease-Activated Receptor-2-Deficient Mice

Lindner

Kahn

Coughlin

et al. 2000

The Journal of Immunology

252

209

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Endothelial surface expression of P-selectin and subsequent leukocyte rolling in venules can be induced by mast cell-derived histamine and binding of thrombin to protease-activated receptor-1 (PAR1). We hypothesized that activation of endothelial PAR2 by mast cell tryptase or other proteases also contributes to inflammatory responses. Leukocyte rolling flux and rolling velocity were assessed by intravital microscopy of the cremaster muscles of wild-type mice following perivenular micropipette injections of a control (LSIGRL) or PAR2-activating (SLIGRL) oligopeptide. Injection of SLIGRL increased mean rolling leukocyte flux fraction from 34 ± 11 to 71 ± 24% (p < 0.05) and decreased mean rolling velocity from 63 ± 29 to 32 ± 2 μm/s (p < 0.05). No significant changes occurred with control peptide injection. To further evaluate the role of PAR2 in inflammatory responses, PAR2-deficient mice were generated by gene targeting and homologous recombination. Perivenular injections of SLIGRL resulted in only a small increase in rolling leukocyte flux fraction (from 21 ± 8 to 30 ± 2%) and no change in rolling velocity. Leukocyte rolling after surgical trauma was assessed in 9 PAR2-deficient and 12 wild-type mice. Early (0–15 min) after surgical trauma, the mean leukocyte rolling flux fraction was lower (10 ± 3 vs 30 ± 6%, p < 0.05) and mean rolling velocity was higher (67 ± 46 vs 52 ± 36 μm/s, p < 0.01) in PAR2-deficient compared with control mice. The defect in leukocyte rolling in PAR2-deficient mice did not persist past 30 min following surgical trauma. These results indicate that activation of PAR2 produces microvascular inflammation by rapid induction of P-selectin-mediated leukocyte rolling. In the absence of PAR2, the onset of inflammation is delayed.

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“…17 Venular diameters were measured off-line with the use of video calipers. Freeze-frame advancing allowed the tracking of individual rolling leukocytes over a distance of 30 to 100 m. The total distance traveled was divided by the elapsed time to derive the mean rolling velocity.…”

Section: Intravital Microscopymentioning

confidence: 99%

Microbubble Persistence in the Microcirculation During Ischemia/Reperfusion and Inflammation Is Caused by Integrin- and Complement-Mediated Adherence to Activated Leukocytes

et al. 2000

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Background-Albumin microbubbles that are used for contrast echocardiography persist within the myocardial microcirculation after ischemia/reperfusion (I-R). The mechanism responsible for this phenomenon is unknown. Methods and Results-Intravital microscopy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice during intravenous injections of fluorescein-labeled microbubbles composed of albumin, anionic lipids, or cationic lipids. Injections were performed at baseline and after 30 to 90 minutes of I-R in 8 mice and 2 hours after intrascrotal tumor necrosis factor-␣ (TNF-␣) in 4 mice. Microbubble adherence at baseline was uncommon (Ͻ2/50 high-power fields). After I-R, adherence increased (PϽ0.05) to 9Ϯ5 and 5Ϯ4 per 50 high-power fields for albumin and anionic lipid microbubbles, respectively, due to their attachment to leukocytes adherent to the venular endothelium. TNF-␣ produced even greater microbubble binding, regardless of the microbubble shell composition. The degree of microbubble attachment correlated (rϭ0.84 to 0.91) with the number of adhered leukocytes. Flow cytometry revealed that microbubbles preferentially attached to activated leukocytes. Albumin microbubble attachment was inhibited by blocking the leukocyte ␤ 2 -integrin Mac-1, whereas lipid microbubble binding was inhibited when incubations were performed in complement-depleted or heat-inactivated serum rather than control serum. Conclusions-Microvascular attachment of albumin and lipid microbubbles in the setting of I-R and TNF-␣-induced inflammation is due to their ␤ 2 -integrin-and complement-mediated binding to activated leukocytes adherent to the venular wall. Thus, microbubble persistence on contrast ultrasonography may be useful for the detection and monitoring of leukocyte adhesion in inflammatory diseases. (Circulation. 2000;101:668-675.)

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Concentration and Velocity Profiles of Blood Cells in the Microcirculation

Cited by 37 publications

References 11 publications

Transit time of leukocytes rolling through venules controls cytokine-induced inflammatory cell recruitment in vivo.

Transit time of leukocytes rolling through venules controls cytokine-induced inflammatory cell recruitment in vivo.

Delayed Onset of Inflammation in Protease-Activated Receptor-2-Deficient Mice

Microbubble Persistence in the Microcirculation During Ischemia/Reperfusion and Inflammation Is Caused by Integrin- and Complement-Mediated Adherence to Activated Leukocytes

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