The Arterial Lumen Is Controlled by Flow-Related Shear Stress

Physiology ◽  
1993 ◽  
Vol 8 (1) ◽  
pp. 34-38 ◽  
Author(s):  
V Smiesko ◽  
PC Johnson
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Blood Flow Velocity ◽  
Flow Regulation ◽  
High Flow ◽  
Normal Flow ◽  
Flow Conditions ◽  
Flow Rates ◽  
Arterial Lumen ◽  
Significant Mechanism

An increase in blood flow velocity through both arteries and arterioles induces a dilation that is mediated by the endothelium. This is a significant mechanism of flow regulation at normal flow rates and is critically important during high flow conditions.

scholarly journals Remodeling of Resistance Arteries in Renal Failure: Effect of Endothelin Receptor Blockade

2001 ◽  
Vol 12 (10) ◽  
pp. 2040-2050 ◽  
Author(s):  
KERSTIN AMANN ◽  
GABRIEL MIL TENBERGER-MIL TENYI ◽  
AURELIA SIMONOVICIENE ◽  
ANDREAS KOCH ◽  
STEPHAN ORTH ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
High Flow ◽  
Mesenteric Arteries ◽  
Low Flow ◽  
Normal Flow ◽  
Flow Conditions ◽  
First Order ◽  
The Media ◽  
Intimal Thickness

Abstract. Remodeling of vessels is a known feature of renal failure, but it is unclear whether this represents an appropriate or inappropriate response to the known changes in blood flow, shear stress, and wall tension. To investigate remodeling in response to variations in blood flow, first-order mesenteric arteries were exposed to high- and low-flow conditions via the ligation of second-order branches, according to the technique described by Pour-ageaud and De Mey. The resulting changes in vessel geometric features, relative proportions of intima and media, submicroscopic structure, and immunostaining for proliferating cell nuclear antigen (PCNA), endothelin-1 (ET-1), and ETAreceptors were assessed in first-order mesenteric arteries under low-flow and high-flow conditions. Subtotally nephrectomized (SNX) animals were compared with sham-operated rats. Animals either were left untreated or were treated with the ETAreceptor antagonist (ET-RA) LU-135252, because of suggestions in the literature that ET is involved in vascular remodeling in uremia. A highly significant increase in intimal thickness was noted in low-flow arteries (4.21 ± 1.39 μm) of SNX animals, compared with normal-flow arteries (2.06 ± 0.61 μm), but this increase was not observed in sham-operated rats (1.38 ± 0.77 in low-flow arteriesversus2.40 ± 0.35 μm in normal-flow arteries). The increase in intimal thickness in low-flow arteries was abrogated by ET-RA. The medial thickness was increased in untreated SNX animals (19.5 ± 3.61 μm), compared with sham-operated rats, and this increase was also prevented by ET-RA. The medial thickness was not affected by low flow in either sham-operated or SNX animals. In parallel, the number of PCNA-positive intimal cells was higher in low-flow, but not high-flow, arteries of SNX rats, compared with sham-operated rats. No significant change was observed in sham-operated animals. In the media, the number of PCNA-positive cells was higher in untreated SNX animals than in sham-operated rats. The number was even more markedly increased in high-flow, but not low-flow, vessels. This increase was abrogated by ET-RA. It is concluded that, in uremic animals, the response of the intima to low flow and the response of the media to high flow are exaggerated. Both responses are apparently mediated by ET.

Derecruitment of filtration surface area in paraquat-injured isolated dog lungs

1990 ◽  
Vol 68 (4) ◽  
pp. 1581-1589 ◽  
Author(s):  
T. Shibamoto ◽  
J. C. Parker ◽  
A. E. Taylor ◽  
M. I. Townsley
Keyword(s):  
Blood Flow ◽  
Surface Area ◽  
Vascular Resistance ◽  
High Flow ◽  
Base Line ◽  
Flow Rates ◽  
Blood Flows ◽  
Capillary Filtration Coefficient ◽  
Specific Index ◽  
Filtration Surface

The capillary filtration coefficient (Kf,c) is a sensitive and specific index of vascular permeability if surface area remains constant, but derecruitment might affect Kf,c in severely damaged lungs with high vascular resistance. We studied the effect of high and low blood flow rates on Kf,c in papaverine-pretreated blood-perfused isolated dog lungs perfused under zone 3 conditions with and without paraquat (PQ, 10(-2) M). Three Kf,cs were measured successively at hourly intervals for 5 h. These progressed sequentially from isogravimetric blood flow with low vascular pressure (I/L) to high flow with low vascular pressure (H/L) to high flow with high vascular pressure (H/H). The blood flows of H/L and H/H were greater than or equal to 1.5 times that of I/L. There were no significant changes in Kf,c in lungs without paraquat over a 50-fold range of blood flow rates. At 3 h after PQ, I/L-Kf,c was significantly increased and both isogravimetric capillary pressure and total protein reflection coefficient were decreased from base line. At 4 and 5 h, H/L-Kf,c was significantly greater than the corresponding I/L-Kf,c (1.01 +/- 0.22 vs. 0.69 +/- 0.09 and 1.26 +/- 0.19 vs. 0.79 +/- 0.10 ml.min-1.cmH2O-1.100 g-1, respectively) and isogravimetric blood flow decreased to 32.0 and 12.0% of base line, respectively. Pulmonary vascular resistance increased to 12 times base line at 5 h after PQ. We conclude that Kf,c is independent of blood flow in uninjured lungs. However, Kf,c measured at isogravimetric blood flow underestimated the degree of increase in Kf,c in severely damaged and edematous lungs because of a high vascular resistance and derecruitment of filtering surface area.

Stimulation of oxygen uptake by glucagon is oxygen dependent in perfused rat liver

1989 ◽  
Vol 256 (2) ◽  
pp. G369-G376
Author(s):  
Z. Kizaki ◽  
R. G. Thurman
Keyword(s):  
Intracellular Calcium ◽  
High Flow ◽  
Perfused Liver ◽  
Normal Flow ◽  
Sprague Dawley ◽  
O2 Uptake ◽  
Intact Cells ◽  
Flow Rates ◽  
Isolated Mitochondria ◽  
Stimulation Of

Livers from well-fed female Sprague-Dawley rats (100-150 g) were perfused at flow rates of 4 or 8 ml.g liver-1.min-1 to deliver O2 to the organ at various rates. During perfusion at normal flow rates (4 ml.g-1.min-1), glucagon (10 nM) increased O2 uptake in perfused liver by approximately 40 mumol.g-1.h-1. In contrast, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 when livers were perfused at high flow rates. Increase in O2 uptake was directly proportional to flow rate and was blocked partially by infusion of phorbol myristate acetate (100 nM) before glucagon. Increase in O2 uptake due to elevated flow was not due to enhanced glucagon delivery, since infusion of 120 nM glucagon at normal flow rates only increased O2 uptake by approximately 40 mumol.g-1.h-1. On the other hand, when O2 tension in the perfusate was manipulated at normal flow rates, the stimulation of O2 uptake by glucagon increased proportional to the average O2 tension in the liver. Infusion of 8-bromo-adenosine 3',5'-cyclic monophosphate (BrcAMP; 25 microM) also increased O2 uptake more than twice as much at high compared with normal flow rates. In the presence of angiotensin II (5 nM), a hormone that increases intracellular calcium, glucagon increased O2 uptake by nearly 100 mumol.g-1.h-1 at normal flow rates. Infusion of glucagon or BrcAMP into livers perfused at normal flow rates increased state 3 rates of O2 uptake of subsequently isolated mitochondria significantly by approximately 25%. In contrast, perfusion with glucagon or BrcAMP at high flow rates increased mitochondrial respiration by 50-60%. Glucagon addition acutely to suspensions of mitochondria, however, had no effect on O2 uptake. These data are consistent with reports that glucagon administration in vivo or treatment of intact cells with glucagon increases O2 uptake of subsequently isolated mitochondria, a phenomenon that can account for the observed increase in O2 uptake in livers perfused at high flow rates with glucagon. Furthermore, these results are consistent with the hypothesis that the effect of glucagon on mitochondria is O2 dependent in the perfused liver. This is most likely due to an effect of intracellular calcium on a mechanism mediated via cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Application of Microfluidic Technology to Evaluate the Influence of Pulsatile Blood Flow On Adhesion of Pediatric Sickle Erytrhocytes

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3238-3238
Author(s):  
WHITE Jennell ◽  
Moira M. Lancelot ◽  
Patrick Hines ◽  
Sharada A. Sarnaik
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Sickle Cell ◽  
Pulsatile Flow ◽  
Contact Time ◽  
Adhesion Assay ◽  
Pulsatile Blood Flow ◽  
Flow Conditions ◽  
Adhesive Properties

Abstract Abstract 3238 Introduction: Sickle cell disease (SCD) is characterized by microvascular occlusion mediated in part by adhesion of sickle erythrocytes (SS RBCs) to the vasculature. Advanced flow adhesion (FA) technology facilitates SS RBC adhesion studies in conditions that simulate in vivo microvascular physiology. Most currently available FA systems measure SS RBC adhesion in non-pulsatile flow conditions, versus pulsatile blood flow conditions generated by the cardiac cycle. The influence of pulsatile blood flow on SS RBC adhesion may be particularly important in pediatric SS RBC adhesion, as children have a broad range of heart rates. This study compares SS RBC adhesion in non-pulsatile and pulsatile flow conditions, utilizing a commercially available, microfluidic FA system. Methods: Peripheral blood was obtained from patients with homozygous SCD (n=7) in steady state (5–18 years) from the Sickle Cell Center at the Children's Hospital of Michigan. FA assays were performed in non-pulsatile and pulsatile flow conditions, at a shear stress of 1.0 dyne/cm2, and increasing shear stress up to 20 dyne/cm2to assess avidity. A programmable control unit regulated pulse frequency, shear stress, and temperature. Adhesion was measured to immobilized human laminin and vascular cell adhesion molecule-1 (VCAM-1). A static adhesion assay was used to assess initrinsic adhesive properties of SS RBCs independent of flow dynamics. Results: Standard assays were performed with 30 mL of isolated SS RBCs (1× 107 cells/mL), and SS RBC adhesion was comparable to levels previously reported in parallel plate flow adhesion assays. FA assays showed that adhesion to both laminin and VCAM-1 was significantly increased in the context of pulsatile blood flow (1.67Hz) compared to non-pulsatile blood flow by 8-fold and 56-fold, respectively. The relationship of SS RBC adhesion to increasing pulse frequencies was variable from patient to patient, although adhesion to both laminin and VCAM-1 was uniformly greater in all pulse frequencies tested (1.0, 1.5, 1.67, and 2.0 Hz) compared to non-pulsatile blood flow. When avidity of adhesion was tested 78% of SS RBCs remained adhered to VCAM-1 at the maximum 20dyne/cm2 shear stress, whereas 6% of SS RBCs remained adhered to laminin at a shear stress of 20 dynes/cm2. Pulsatile adhesion to VCAM-1 and laminin was unaffected by protein kinase A (PKA) inhibition, although adhesion to laminin decreased by 31% in one of three patients. To determine if increased adhesion under pulse-flow conditions was due to increased contact time with the immobilized substrate versus a change in the SS RBC's intrinsic adhesive state, we measured SS RBC adhesion in a static adhesion assay following exposure to pulsatile versus non-pulsatile conditions. There was no significant difference in static adhesion to VCAM-1, however adhesion of pulse-exposed SS RBCs to laminin was more variable. Static adhesion of pulse-exposed SS RBCs to laminin was reduced by 60% in the presence of a PKA inhibitor. Conclusions: Our data demonstrate the application of a commercially available microfluidic flow adhesion assay system for efficient assessment of SS RBC adhesive properties. In the future, such advances may allow SS RBC adhesive properties to be evaluated clinically as a predictive tool for future vaso-occlusive events, and to predict individual patient response to anti-adhesive therapy. The small volume of blood required makes this system particularly attractive for studying pediatric samples. Additionally, our data demonstrate that adhesion to both an endothelial cell substrate (VCAM-1) and a subendothelial matrix substrate (laminin) is significantly influenced by the presence of pulsatile blood flow. Although PKA may play a minor role in pulsatile adhesion to laminin, increased contact time with immobilized laminin and VCAM-1 may be a greater contributor to increased adhesion under pulsatile conditions versus non-pulsatile conditions. Pediatric SS RBCs adhered to VCAM at higher levels and with more avidity compared to laminin. The pulsatile flow conditions described in this study more closely approximate in vivo microvascular conditions compared to non-pulsatile conditions commonly used to study SS RBC adhesion. Based on these differences in adhesion under pulsatile versus non-pulsatile flow, incorporating pulsatile flow in future adhesion studies may be more representative of in vivo conditions. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Increased Inlet Blood Flow Velocity Predicts Low Wall Shear Stress in the Cephalic Arch of Patients with Brachiocephalic Fistula Access

PLoS ONE ◽  
2016 ◽  
Vol 11 (4) ◽  
pp. e0152873 ◽  
Author(s):  
Mary Hammes ◽  
Michael Boghosian ◽  
Kevin Cassel ◽  
Sydeaka Watson ◽  
Brian Funaki ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Wall Shear ◽  
Brachiocephalic Fistula

Plasma viscosity and cerebral blood flow

2000 ◽  
Vol 279 (4) ◽  
pp. H1949-H1954 ◽  
Author(s):  
Yoshinobu Tomiyama ◽  
Johnny E. Brian ◽  
Michael M. Todd
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Blood Cells ◽  
Exchange Transfusion ◽  
Ringer Solution ◽  
Plasma Viscosity ◽  
High Flow ◽  
Flow Conditions ◽  
Whole Blood Viscosity

We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on “baseline” CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H2 clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 ± 10.2 ml · 100 g−1 · min−1 (±SD). In control animals, changing plasma viscosity to 1.0 or 3.0 cP resulted in CBF of 55.9 ± 8.6 and 42.5 ± 12.7 ml · 100 g−1 · min−1, respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1.0 cP, CBF varied from 98 to 115 ml · 100 g−1 · min−1. When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml · 100 g−1 · min−1 and was significantly reduced in each case ( P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.

Sensitivity of patient-specific numerical simulation of cerebal aneurysm hemodynamics to inflow boundary conditions

2007 ◽  
Vol 106 (6) ◽  
pp. 1051-1060 ◽  
Author(s):  
Prem Venugopal ◽  
Daniel Valentino ◽  
Holger Schmitt ◽  
J. Pablo Villablanca ◽  
Fernando Viñuela ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Boundary Conditions ◽  
Numerical Simulations ◽  
Flow Rate ◽  
Artery Aneurysm ◽  
Blood Flow Rate ◽  
Patient Specific ◽  
Stress Distributions ◽  
Flow Rates

Object Due to the difficulty of obtaining patient-specific velocity measurements during imaging, many assumptions have to be made while imposing inflow boundary conditions in numerical simulations conducted using patient-specific, imaging-based cerebral aneurysm models. These assumptions can introduce errors, resulting in lack of agreement between the computed flow fields and the true blood flow in the patient. The purpose of this study is to evaluate the effect of the assumptions made while imposing inflow boundary conditions on aneurysmal hemodynamics. Methods A patient-based anterior communicating artery aneurysm model was selected for this study. The effects of various inflow parameters on numerical simulations conducted using this model were then investigated by varying these parameters over ranges reported in the literature. Specifically, we investigated the effects of heart and blood flow rates as well as the distribution of flow rates in the A1 segments of the anterior cerebral artery. The simulations revealed that the shear stress distributions on the aneurysm surface were largely unaffected by changes in heart rate except at locations where the shear stress magnitudes were small. On the other hand, the shear stress distributions were found to be sensitive to the ratio of the flow rates in the feeding arteries as well as to variations in the blood flow rate. Conclusions Measurement of the blood flow rate as well as the distribution of the flow rates in the patient's feeding arteries may be needed for numerical simulations to accurately reproduce the intraaneurysmal hemodynamics in a specific aneurysm in the clinical setting.

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