Regulation of flow and wall shear stress in arteriolar  networks of the hamster cheek pouch

Our purpose was to define arteriolar network hemodynamics during moderate increases in interstitial adenosine or nitric oxide in the hamster ( n = 34, pentobarbital sodium 70 mg/kg) cheek pouch tissue. The network consists of a feed arteriole (∼12-μm diameter, ∼800-μm length) with three to six branches. Observations of diameter, red blood cell flux, and velocity were obtained at the feed before the branch and within the branch. A comparison of baseline with suffused adenosine or sodium nitroprusside (SNP) 10−9 to 10−5 M showed the following. First, diameter change was heterogeneous by agonist, did not reflect the expected dilatory response, and was related to location within the network. With adenosine, upstream branch points constricted and those downstream dilated, even at 10−5 M. With SNP, upstream branch points dilated, whereas those downstream constricted. Second, with adenosine, changes in diameter, flux, and velocity together resulted in no change in wall shear stress until 10−5 M. Wall shear stress was not maintained at a constant level with N ω-nitro-l-arginine (10−5 M), suggesting a role for flow-dependent diameter changes with adenosine. With SNP, diameter change correlated with the baseline (before SNP) shear stress conditions.

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Influence of Intermittent Pneumatic Compression on Wall Shear Stress and Nitric Oxide Levels

ASME 2011 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2011-53670 ◽

2011 ◽

Author(s):

Ganesh Swaminathan ◽

Suraj Thyagaraj ◽

Francis Loth ◽

Susan McCormick ◽

Hisham Bassiouny

Keyword(s):

Nitric Oxide ◽

Shear Stress ◽

Wall Shear Stress ◽

Blood Vessels ◽

Healthy Subjects ◽

Vascular Diseases ◽

Intermittent Pneumatic Compression ◽

Peripheral Vascular ◽

Peripheral Vascular Diseases ◽

Wall Shear

Wall shear stress (WSS) in blood vessels has been shown to play an important role in the development of atherosclerosis. In particular, regions of low and oscillating WSS have been shown to correlate with the localization of atherosclerosis. Thus, we hypothesize that increasing the WSS for patients with peripheral vascular diseases (PVD) will either reduce PVD severity or slow its progression. We analyzed WSS changes from a study by Delis et al. on 32 limbs of PVD patients [1]. Results show that intermittent pneumatic compression (IPC) increases mean WSS by 170% and 240% in PVD patients and healthy subjects, respectively. Peak WSS was found to increase by 93% and 40% in PVD patients and healthy subjects, respectively. In addition, we examined changes in NOX level with use of IPC on five limbs from PVD patients. Our study demonstrated increased NOx levels in subjects after IPC. Further research is needed to determine the benefits of IPC for PVD patients.

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Effect of Reynolds number and flow division on patterns of haemodynamic wall shear stress near branch points in the descending thoracic aorta

Journal of The Royal Society Interface ◽

10.1098/rsif.2008.0323 ◽

2008 ◽

Vol 6 (35) ◽

pp. 539-548 ◽

Cited By ~ 15

Author(s):

A. Kazakidi ◽

S.J. Sherwin ◽

P.D. Weinberg

Keyword(s):

Reynolds Number ◽

Shear Stress ◽

Wall Shear Stress ◽

Thoracic Aorta ◽

Flow Region ◽

Side Branch ◽

Branch Points ◽

Atherosclerotic Lesions ◽

Wall Shear ◽

Flow Division

Atherosclerotic lesions are non-uniformly distributed at arterial bends and branch sites, suggesting an important role for haemodynamic factors, particularly wall shear stress (WSS), in their development. The pattern of lesions at aortic branch sites depends on age and species. Using computational flow simulations in an idealized model of an intercostal artery emerging perpendicularly from the thoracic aorta, we studied the effects of Reynolds number and flow division under steady conditions. Patterns of flow and WSS were strikingly dependent on these haemodynamic parameters. With increasing Reynolds number, WSS, normalized by the fully developed aortic value, was lowered at the sides of the ostium and increased upstream and downstream of it. Increasing flow into the side branch exacerbated these patterns and gave rise to a reversing flow region downstream of the ostium. Incorporation of more realistic geometric features had only minor effects and patterns of mean WSS under pulsatile conditions were similar to the steady flow results. Aspects of the observed WSS patterns correlate with, and may explain, some but not all of the lesion patterns in human, rabbit and mouse aortas.

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Reverse arterial wall shear stress causes nitric oxide-dependent vasodilatation in the anaesthetised dog

Pflügers Archiv - European Journal of Physiology ◽

10.1007/s00424-002-0915-9 ◽

2002 ◽

Vol 445 (1) ◽

pp. 51-54 ◽

Cited By ~ 10

Author(s):

Markos F. ◽

Hennessy B. ◽

Fitzpatrick M. ◽

O'Sullivan J. ◽

Snow H.

Keyword(s):

Nitric Oxide ◽

Shear Stress ◽

Wall Shear Stress ◽

Arterial Wall ◽

Wall Shear

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Corelease of nitric oxide and prostaglandins mediates flow-dependent dilation of rat gracilis muscle arterioles

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h326 ◽

1994 ◽

Vol 267 (1) ◽

pp. H326-H332 ◽

Cited By ~ 72

Author(s):

A. Koller ◽

D. Sun ◽

A. Huang ◽

G. Kaley

Keyword(s):

Nitric Oxide ◽

Shear Stress ◽

Wall Shear Stress ◽

Gracilis Muscle ◽

Combined Application ◽

Perfusate Flow ◽

Factor Inhibitor ◽

Flow Shear Stress ◽

Wall Shear ◽

Oxide Synthase

We have studied the mechanisms responsible for the mediation of flow (shear stress)-induced dilation of isolated arterioles of rat gracilis muscle. Active diameter of arterioles at a constant perfusion pressure (PP, 80 mmHg) was approximately 92 microns, while their passive diameter (Ca(2+)-free solution) was approximately 165 microns. At a constant PP the stepwise increase in flow of the perfusion solution (PS, 0-60 microliters/min in 10-microliters/min steps) elicited a gradual increase in diameter up to approximately 140 microns. Flow-induced dilations were eliminated by the removal of the endothelium of arterioles (by air). Dilations were significantly reduced by the cyclooxygenase blocker, indomethacin (Indo, 10(-5) M), by the nitric oxide synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), or by the endothelium-derived relaxing factor inhibitor, oxyhemoglobin (Hb, 10(-5) M), as indicated by the significant changes in the slope of the regression lines of the flow-diameter curves. For example, during administration of the inhibitors, dilation to 60 microliters/min perfusate flow was reduced by 41.1, 54.3, and 39.3%, respectively. Combined application of Indo and L-NNA almost completely eliminated flow-induced dilation. Arteriolar dilation maintained calculated wall shear stress close to control values (approximately 30 dyn/cm2 at 60 microliters/min) despite increases in flow, but when the dilation was inhibited by removal of the endothelium or by the combined administration of Indo and L-NNA, wall shear stress was greatly increased as a function of increases in flow of the PS (approximately 125 dyn/cm2).(ABSTRACT TRUNCATED AT 250 WORDS)

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MICROVASCULAR FLOW AND WALL SHEAR STRESS DURING INTRAVENOUS NITRIC OXIDE DONORS

Anesthesiology ◽

10.1097/00000542-199809120-00015 ◽

1998 ◽

Vol 89 (Supplement) ◽

pp. 603A

Author(s):

S. Shahzad Mustafa ◽

Richard J. Rivers ◽

Mary D.S. Frame

Keyword(s):

Nitric Oxide ◽

Shear Stress ◽

Wall Shear Stress ◽

Nitric Oxide Donors ◽

Microvascular Flow ◽

Wall Shear

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Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01371.2007 ◽

2008 ◽

Vol 294 (4) ◽

pp. H1914-H1922 ◽

Cited By ~ 18

Author(s):

Silvia Bertuglia

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Shear Stress ◽

Intermittent Hypoxia ◽

Ischemia Reperfusion ◽

Thiobarbituric Acid ◽

Cheek Pouch ◽

Capillary Perfusion ◽

Hamster Cheek Pouch ◽

Arterial Blood

The microvascular function of nitric oxide (NO) during ischemia-reperfusion (I/R) in intermittent hypoxia (IH)-pretreated hamsters was analyzed using 20 mg/kg of the nonselective NO inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) and 5 mg/kg of the preferential inducible NO inhibitor S-methylisothiourea sulphate (SMT) injected before I/R. Studies were made in the hamster cheek pouch microcirculation (intravital fluorescence microscopy). IH consisted of 6 min of 8% O2breathing followed by 6 min of 21% O2for every 8 h for 21 days. Normoxia controls (NCs) were exposed to room air for the same period. The effects were characterized in terms of systemic hemodynamics, diameter, flow, wall shear stress in arterioles, capillary perfusion, and the concentrations of thiobarbituric acid-reactive substances (TBARS) and plasma NO, assessed as nitrite/nitrate (NOx) levels. IH did not change arterial blood pressure and increased hematocrit and shear stress. IH increased NOx and TBARS levels and reduced arterial diameter, blood flow, and capillary perfusion versus the NC. Conversely, TBARS and NOx were lower during I/R in IH-pretreated hamsters, resulting in vasodilation and the increase of capillary perfusion and shear stress. After IH, capillary perfusion was reduced by 24% (2.3%) and enhanced by 115% (1.7%) after I/R ( P < 0.05). Both modalities of NO blockade decreased NOx generation and increased TBARS versus IH. l-NAME and SMT induced a significant decrease in arteriolar diameter, blood flow, and capillary perfusion ( P < 0.05). l-NAME enhanced TBARS more than SMT and aggravated I/R damage. In conclusion, we demonstrated that preconditioning with IH greatly reduces oxidative stress and stimulates NO-induced vasodilation during I/R injury, thus maintaining capillary perfusion.

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