Retrograde Flow and Shear Rate Acutely Impair Endothelial Function in Humans

Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to ex...

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Published inHypertension (Dallas, Tex. 1979) Vol. 53; no. 6; pp. 986 - 992
Main Authors Thijssen, Dick H.J, Dawson, Ellen A, Tinken, Toni M, Cable, N Timothy, Green, Daniel J
Format Journal Article
LanguageEnglish
Published Hagerstown, MD American Heart Association, Inc 01.06.2009
Lippincott Williams & Wilkins
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Abstract Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24±3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in “dose”-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P<0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P<0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P=0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
AbstractList Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24±3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in “dose”-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects ( P <0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions ( P <0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention ( P =0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24+/-3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in "dose"-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P&lt;0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P&lt;0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P=0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24+/-3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in "dose"-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P<0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P<0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P=0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear can occur through human conduit arteries. In animals, retrograde shear is associated with atherogenic effects. The aim of this study was to examine the impact of incremental levels of retrograde shear on endothelial function in vivo. On 3 separate days, we examined bilateral brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men (24±3 years) before and after a 30-minute intervention consisting of cuff inflation to 25, 50, or 75 mm Hg. Cuff inflations resulted in “dose”-dependent increases in retrograde shear rate, compared with the noncuffed arm, within subjects (P<0.001). Flow-mediated dilation in the cuffed arm did not change in response to the 25-mm Hg stimulus but decreased significantly after both the 50- and 75-mm Hg interventions (P<0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (P=0.03). In the noncuffed arm, no changes in shear rate or flow-mediated dilation were observed. These results demonstrate that an increase in retrograde shear rate induces a dose-dependent attenuation of endothelial function in humans. This finding contributes to our understanding regarding the possible detrimental effects of retrograde shear rate in vivo.
Author Tinken, Toni M
Green, Daniel J
Dawson, Ellen A
Thijssen, Dick H.J
Cable, N Timothy
AuthorAffiliation From the Research Institute for Sport and Exercise Science (D.H.J.T., E.A.D., T.M.T., N.T.C., D.J.G.), Liverpool John Moores University, Liverpool, United Kingdom; Department of Physiology (D.H.J.T.), Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; and the School of Sport Science (D.J.G.), Exercise and Health, University of Western Australia, Crawley, Western Australia, Australia
AuthorAffiliation_xml – name: From the Research Institute for Sport and Exercise Science (D.H.J.T., E.A.D., T.M.T., N.T.C., D.J.G.), Liverpool John Moores University, Liverpool, United Kingdom; Department of Physiology (D.H.J.T.), Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; and the School of Sport Science (D.J.G.), Exercise and Health, University of Western Australia, Crawley, Western Australia, Australia
Author_xml – sequence: 1
  givenname: Dick
  surname: Thijssen
  middlename: H.J
  fullname: Thijssen, Dick H.J
  organization: From the Research Institute for Sport and Exercise Science (D.H.J.T., E.A.D., T.M.T., N.T.C., D.J.G.), Liverpool John Moores University, Liverpool, United Kingdom; Department of Physiology (D.H.J.T.), Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; and the School of Sport Science (D.J.G.), Exercise and Health, University of Western Australia, Crawley, Western Australia, Australia
– sequence: 2
  givenname: Ellen
  surname: Dawson
  middlename: A
  fullname: Dawson, Ellen A
– sequence: 3
  givenname: Toni
  surname: Tinken
  middlename: M
  fullname: Tinken, Toni M
– sequence: 4
  givenname: N
  surname: Cable
  middlename: Timothy
  fullname: Cable, N Timothy
– sequence: 5
  givenname: Daniel
  surname: Green
  middlename: J
  fullname: Green, Daniel J
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21539879$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/19380611$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2009 American Heart Association, Inc.
2009 INIST-CNRS
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Issue 6
Keywords Doppler ultrasound study
Human
Hypertension
endothelial function
Shear
retrograde shear stress
Shear stress
Cardiovascular disease
oscillatory
shear stress pattern
echo Doppler
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PublicationTitle Hypertension (Dallas, Tex. 1979)
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Lippincott Williams & Wilkins
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Snippet Changes in arterial shear stress induce functional and structural vasculature adaptations. Recent studies indicate that substantial retrograde flow and shear...
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SubjectTerms Adult
Analysis of Variance
Area Under Curve
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Flow Velocity - physiology
Blood Pressure Determination - methods
Brachial Artery - physiology
Cardiology. Vascular system
Endothelium, Vascular - physiopathology
Experimental diseases
Forearm - blood supply
Humans
Male
Medical sciences
Muscle Contraction - physiology
Muscle, Smooth, Vascular - physiology
Probability
Reference Values
Risk Factors
Sampling Studies
Sensitivity and Specificity
Shear Strength - physiology
Vasoconstriction - physiology
Vasodilation - physiology
Young Adult
Title Retrograde Flow and Shear Rate Acutely Impair Endothelial Function in Humans
URI https://www.ncbi.nlm.nih.gov/pubmed/19380611
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