Effect of Cell-Free Layer Variation on Arteriolar Wall Shear Stress

Using a simplified two-dimensional divider-channel setup, we simulate the development process of red blood cell (RBC) flows in the entrance region of microvessels to study the wall shear stress (WSS) behaviors. Significant temporal and spatial variation in WSS is noticed. The maximum WSS magnitude and the strongest variation are observed at the channel inlet due to the close cell-wall contact. From the channel inlet, both the mean WSS and variation magnitude decrease, with a abrupt drop in the close vicinity near the inlet and then a slow relaxation over a relatively long distance; and a relative stable state with approximately constant mean and variation is established when the flow is well developed. The correlations between the WSS variation features and the cell free layer (CFL) structure are explored, and the effects of several hemodynamic parameters on the WSS variation are examined. In spite of the model limitations, the qualitative information revealed in this study could be useful for better understanding relevant processes and phenomena in the microcirculation.

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Oxygen release from arterioles with normal flow and no-flow conditions

Journal of Applied Physiology ◽

10.1152/japplphysiol.00762.2005 ◽

2006 ◽

Vol 100 (5) ◽

pp. 1569-1576 ◽

Cited By ~ 12

Author(s):

Pedro Cabrales ◽

Amy G. Tsai ◽

Paul C. Johnson ◽

Marcos Intaglietta

Keyword(s):

Shear Stress ◽

Wall Shear Stress ◽

Vessel Wall ◽

Oxygen Release ◽

Flow Conditions ◽

Phosphorescence Quenching ◽

Dextran 70 ◽

Lower Oxygen ◽

Arteriolar Wall ◽

Wall Shear

The rate of oxygen release from arterioles (∼55 μm diameter) was measured in the hamster window chamber model during flow and no-flow conditions. Flow was stopped by microvascular transcutaneous occlusion using a glass pipette held by a manipulator. The reduction of the intra-arteriolar oxygen tension (Po2) was measured by the phosphorescence quenching of preinfused Pd-porphyrin, 100 μm downstream from the occlusion. Oxygen release from arterioles was found to be 53% greater during flow than no-flow conditions (2.6 vs. 1.7 × 10−5 ml O2·cm−2·s−1, P < 0.05). Acute hemodilution with dextran 70 was used to reduce vessel oxygen content, significantly increase wall shear stress (14%, P < 0.05), reduce Hct to 28.4% (SD 1.0) [vs. 48.8% (SD 1.8) at baseline], lower oxygen supply by the arterioles (10%, P < 0.05), and increase oxygen release from the arterioles (39%, P < 0.05). Hemodilution also increased microcirculation oxygen extraction (33% greater than nonhemodilution, P < 0.05) and oxygen consumption by the vessel wall, as shown by an increase in vessel wall oxygen gradient [difference in Po2 between the blood and the tissue side of the arteriolar wall, nonhemodiluted 16.2 Torr (SD 1.0) vs. hemodiluted 18.3 Torr (SD 1.4), P < 0.05]. Oxygen released by the arterioles during flow vs. nonflow was increased significantly after hemodilution (3.6 vs. 1.8 × 10−5 ml O2·cm−2·s−1, P < 0.05). The oxygen cost induced by wall shear stress, suggested by our findings, may be >15% of the total oxygen delivery to tissues by arterioles during flow in this preparation.

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Oxidative stress-induced dysregulation of arteriolar wall shear stress and blood pressure in hyperhomocysteinemia is prevented by chronic vitamin C treatment

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00448.2003 ◽

2003 ◽

Vol 285 (6) ◽

pp. H2277-H2283 ◽

Cited By ~ 34

Author(s):

Zsolt Bagi ◽

Csongor Csekö ◽

Erika Tóth ◽

Akos Koller

Keyword(s):

Oxidative Stress ◽

Blood Pressure ◽

Shear Stress ◽

Wall Shear Stress ◽

Vitamin C ◽

Arterial Blood ◽

Control Serum ◽

Arteriolar Wall ◽

Wall Shear

We aimed to test the hypothesis that an enhanced level of reactive oxygen species (ROS) is primarily responsible for the impairment of nitric oxide (NO)-mediated regulation of arteriolar wall shear stress (WSS) in hyperhomocysteinemia (HHcy). Thus flow/WSS-induced dilations of pressurized gracilis muscle arterioles (basal diameter: ∼170 μm) isolated from control (serum Hcy: 6 ± 1 μM), methionine diet-induced HHcy rats (4 wk, serum Hcy: 30 ± 6 μM), and HHcy rats treated with vitamin C, a known antioxidant (4 wk, 150 mg · kg body wt–1 · day–1; serum Hcy: 32 ± 10 μM), were investigated. In vessels of HHcy rats, increases in intraluminal flow/WSS-induced dilations were converted to constrictions. Constrictions were unaffected by inhibition of NO synthesis by Nω-nitro-l-arginine methyl ester (l-NAME). Vitamin C treatment of HHcy rats reversed the WSS-induced arteriolar constrictions to l-NAME-sensitive dilations but did not affect control responses. Similar changes in responses were obtained for the calcium ionophore A-23187. In addition, diastolic and mean arterial blood pressure and serum 8-isoprostane levels (a marker of in vivo oxidative stress) were significantly elevated in rats with HHcy, changes that were normalized by vitamin C treatment. Taken together, our data show that in chronic HHcy long-term vitamin C treatment, by decreasing oxidative stress in vivo, enhanced NO bioavailability, restored the regulation of shear stress in arterioles, and normalized systemic blood pressure. Thus our study provides evidence that oxidative stress is an important in vivo mechanism that is primarily responsible for the development of endothelial dysregulation of WSS in HHcy.

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