scholarly journals Flow-mediated dilation stimulated by sustained increases in shear stress: A useful tool for assessing endothelial function in humans?

2017 ◽  
pp. ajpheart.00534. ◽  
Author(s):  
Joshua C Tremblay ◽  
Kyra Ellen Pyke
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Flow Mediated Dilation

scholarly journals Endothelial dysfunction following prolonged sitting is mediated by a reduction in shear stress

2016 ◽  
Vol 310 (5) ◽  
pp. H648-H653 ◽  
Author(s):  
Robert M. Restaino ◽  
Lauren K. Walsh ◽  
Takuma Morishima ◽  
Jennifer R. Vranish ◽  
Luis A. Martinez-Lemus ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Internal Control ◽  
Popliteal Artery ◽  
Local Heating ◽  
Underlying Mechanism ◽  
Flow Mediated Dilation ◽  
Prolonged Sitting ◽  
Artery Flow

We and others have recently reported that prolonged sitting impairs endothelial function in the leg vasculature; however, the mechanism(s) remain unknown. Herein, we tested the hypothesis that a sustained reduction in flow-induced shear stress is the underlying mechanism by which sitting induces leg endothelial dysfunction. Specifically, we examined whether preventing the reduction in shear stress during sitting would abolish the detrimental effects of sitting on popliteal artery endothelial function. In 10 young healthy men, bilateral measurements of popliteal artery flow-mediated dilation were performed before and after a 3-h sitting period during which one foot was submerged in 42°C water (i.e., heated) to increase blood flow and thus shear stress, whereas the contralateral leg remained dry and served as internal control (i.e., nonheated). During sitting, popliteal artery mean shear rate was reduced in the nonheated leg (pre-sit, 42.9 ± 4.5 s−1; and 3-h sit, 23.6 ± 3.3 s−1; P < 0.05) but not in the heated leg (pre-sit, 38.9 ± 3.4 s−1; and 3-h sit, 63.9 ± 16.9 s−1; P > 0.05). Popliteal artery flow-mediated dilation was impaired after 3 h of sitting in the nonheated leg (pre-sit, 7.1 ± 1.4% vs. post-sit, 2.8 ± 0.9%; P < 0.05) but not in the heated leg (pre-sit: 7.3 ± 1.5% vs. post-sit, 10.9 ± 1.8%; P > 0.05). Collectively, these data suggest that preventing the reduction of flow-induced shear stress during prolonged sitting with local heating abolishes the impairment in popliteal artery endothelial function. Thus these findings are consistent with the hypothesis that sitting-induced leg endothelial dysfunction is mediated by a reduction in shear stress.

scholarly journals UBC-Nepal expedition: upper and lower limb conduit artery shear stress and flow-mediated dilation on ascent to 5,050 m in lowlanders and Sherpa

2018 ◽  
Vol 315 (6) ◽  
pp. H1532-H1543 ◽  
Author(s):  
Joshua C. Tremblay ◽  
Ryan L. Hoiland ◽  
Howard H. Carter ◽  
Connor A. Howe ◽  
Mike Stembridge ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
High Altitude ◽  
Blood Viscosity ◽  
Lower Limb ◽  
Adaptation To Hypoxia ◽  
Flow Mediated Dilation ◽  
Conduit Artery ◽  
Arterial Blood ◽  
Retrograde Shear

The study of conduit artery endothelial adaptation to hypoxia has been restricted to the brachial artery, and comparisons with highlanders have been confounded by differences in altitude exposure, exercise, and unknown levels of blood viscosity. To address these gaps, we tested the hypothesis that lowlanders, but not Sherpa, would demonstrate decreased mean shear stress and increased retrograde shear stress and subsequently reduced flow-mediated dilation (FMD) in the upper and lower limb conduit arteries on ascent to 5,050 m. Healthy lowlanders (means ± SD, n = 22, 28 ± 6 yr) and Sherpa ( n = 12, 34 ± 11 yr) ascended over 10 days, with measurements taken on nontrekking days at 1,400 m (baseline), 3,440 m ( day 4), 4,371 m ( day 7), and 5,050 m ( day 10). Arterial blood gases, blood viscosity, shear stress, and FMD [duplex ultrasound of the brachial and superficial femoral arteries (BA and SFA, respectively)] were acquired at each time point. Ascent decreased mean and increased retrograde shear stress in the upper and lower limb of lowlanders and Sherpa. Although BA FMD decreased in lowlanders from 7.1 ± 3.9% to 3.8 ± 2.8% at 5,050 versus 1,400 m ( P < 0.001), SFA FMD was preserved. In Sherpa, neither BA nor SFA FMD were changed upon ascent to 5,050 m. In lowlanders, the ascent-related exercise may favorably influence endothelial function in the active limb (SFA); selective impairment in FMD in the BA in lowlanders is likely mediated via the low mean or high oscillatory baseline shear stress. In contrast, Sherpa presented protected endothelial function, suggesting a potential vascular aspect of high-altitude acclimatization/adaptation. NEW & NOTEWORTHY Upper and lower limb arterial shear stress and flow-mediated dilation (FMD) were assessed on matched ascent from 1,400 to 5,050 m in lowlanders and Sherpa. A shear stress pattern associated with vascular dysfunction/risk manifested in both limbs of lowlanders and Sherpa. FMD was impaired only in the upper limb of lowlanders. The findings indicate a limb-specific impact of high-altitude trekking on FMD and a vascular basis to acclimatization wherein endothelial function is protected in Sherpa on ascent

Evidence of a limb- and shear stress stimulus profile-dependent impact of high-intensity cycling training on flow-mediated dilation

2020 ◽  
Vol 45 (2) ◽  
pp. 135-145
Author(s):  
Trevor J. King ◽  
Kyra E. Pyke
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Endurance Training ◽  
Training Group ◽  
Lower Limbs ◽  
Stress Profile ◽  
Flow Mediated Dilation ◽  
Post Intervention ◽  
The Impact ◽  
Cycling Training

Lower limb endurance training can improve conduit artery flow-mediated dilation (FMD) in response to transient increases in shear stress (reactive hyperemia; RH-FMD) in both the upper and lower limbs. Sustained increases in shear stress recruit a partially distinct transduction pathway and elicit a physiologically relevant FMD response (SS-FMD) that provides distinct information regarding endothelial function. However, the impact of training on SS-FMD is not well understood. The purpose of this study was to determine the impact of cycling training on handgrip exercise-induced brachial artery (BA) FMD (BA SS-FMD) and calf plantar-flexion-induced superficial femoral artery (SFA) FMD (SFA SS-FMD). RH-FMD was also assessed in both arteries. Twenty-eight young males were randomized to control (n = 12) or training (n = 16) groups. The training group cycled 30 min/day, 3 days/week for 4 weeks at 80% heart rate reserve. FMD was assessed in the BA and SFA before and after the intervention via Duplex ultrasound. Results are means ± SD. Training did not impact SS-FMD in either artery, and SFA RH-FMD was also unchanged (p > 0.05). When controlling for the shear rate stimulus via covariate analysis, BA RH-FMD improved in the training group (p = 0.05) (control – pre-intervention: 5.7% ± 2.4%, post-intervention: 5.3% ± 2.4%; training – pre-intervention: 5.4% ± 2.5%, post-intervention: 7.2% ± 2.4%). Thus, endurance training resulted in nonuniform adaptations to endothelial function, with an isolated impact on the BA’s ability to transduce a transient increase in shear stress. Novelty Training did not alter SS-FMD in the arm or leg. RH-FMD was augmented in the arm only. Thus training adaptations were limb- and shear stress profile-specific.

Abstract 377: Retrograde Shear Stress does not Alter Endothelial Function in Healthy Subjects

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Sooraj Shah ◽  
Stuart Katz
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Healthy Subjects ◽  
Flow Mediated Dilation ◽  
Retrograde Flow ◽  
Experimental Conditions ◽  
Before And After ◽  
Arm Elevation ◽  
The Difference ◽  
Retrograde Shear

Introduction: Endothelial dysfunction is a precursor and plays a significant role in development of atherosclerosis. Retrograde flow and resulting retrograde shear stress has been shown to adversely affect the endothelial function but the results may be flawed due to experimental conditions. Change in the limb position might result in increase in retrograde flow and adversely affect endothelial function. We hypothesized that elevation of arm above the level of the heart will result in increased retrograde flow and reduced endothelial function as measured by flow mediated dilation (FMD). Methods: We enrolled 27 healthy subjects after obtaining informed consent. Endothelial function was measured by FMD in brachial artery before and after arm elevation with elbow support for 30 minutes in fasting state. Flow velocities were recorded and analyzed at baseline, 10 and 20 minutes after arm elevation and at the end of 30 minutes. Results: The mean retrograde flow velocity was 9.9 ± 7.75 cm/sec at baseline, which increased to 15.8 ± 6.56 cm/sec (p=0.0019) after arm elevation. Out of the 27 subjects 21 (78%) subjects had increase in retrograde flow (20% or more). The difference in FMD change between the groups with increased or no change in retrograde flow was statistically non-significant (p=0.4). Conclusion: In conclusion arm elevation for 30 minutes was associated with statistically significant increase in retrograde flow without significant change in endothelial function in normal healthy subjects. The change in endothelial function between subjects who had augmented retrograde shear and those who did not was statistically not significant.

scholarly journals Examining the acute effects of retrograde versus low mean shear rate on flow-mediated dilation

2019 ◽  
Vol 126 (5) ◽  
pp. 1335-1342 ◽  
Author(s):  
Joshua C. Tremblay ◽  
Arman S. Grewal ◽  
Kyra E. Pyke
Keyword(s):  
Shear Stress ◽  
Shear Rate ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Duplex Ultrasound ◽  
Flow Mediated Dilation ◽  
Relative Contribution ◽  
Stress Components ◽  
Retrograde Shear

Arterial endothelial function is acutely and chronically regulated by blood flow-associated shear stress. An acute intervention employing modest forearm cuff occlusion to simultaneously increase retrograde and decrease mean brachial artery shear rate for 30 min evokes transient impairments in flow-mediated dilation (FMD). However, the independent influence of the low mean versus the retrograde shear stress components is unclear. Healthy young adults [ n = 24 (12 women, 12 men); 22 ± 2 yr, body mass index = 25 ± 2 kg/m2 (mean ± SD)] completed three laboratory visits within 1 wk. Visits consisted of 45 min of supine rest followed by a brachial artery FMD test (duplex ultrasound) before and after a 30-min intervention: control (shear rate unchanged), cuff (mean shear rate decreased, retrograde shear rate increased), or arterial compression (mean shear rate decreased, no increase in retrograde shear rate). The mean shear rate on the compression visit was targeted to match that achieved on the cuff visit. Cuff and compression trials decreased mean shear rate to a similar extent (cuff: 43 ± 22 s−1, compression: 43 ± 21 s−1; P = 0.850) compared with control (65 ± 21 s−1; both P < 0.001), with the retrograde component elevated only in the former (cuff: −83 ± 30 s−1, compression: −7 ± 5 s−1; P < 0.001). FMD decreased by 29 ± 30% ( P < 0.001) after the cuff intervention and 32 ± 24% ( P < 0.001) after the compression trial but was unchanged on the control visit (−0.3 ± 18%; P = 0.754). This was not altered by accounting for the shear rate stimulus. An increased retrograde shear stress does not appear to be obligatory for the transient reduction in FMD achieved after a 30-min exposure to low mean shear stress. These findings provide novel mechanistic insight on the regulation of endothelial function in vivo. NEW & NOTEWORTHY Low mean and retrograde shear stress are considered atherogenic; however, their relative contribution to the acute regulation of endothelial function in humans is unclear. Matched reductions in mean shear stress (30 min), with and without increases in retrograde shear stress, elicited equivalent reductions in flow-mediated dilation in men and women. These findings afford novel insight regarding the shear stress components governing the acute (dys)regulation of conduit artery endothelial function in vivo.

Endothelial function and shear stress in hypobaric hypoxia: time course and impact of plasma volume expansion in men

2020 ◽  
Vol 319 (5) ◽  
pp. H980-H994
Author(s):  
Joshua C. Tremblay ◽  
Philip N. Ainslie ◽  
Rachel Turner ◽  
Hannes Gatterer ◽  
Maja Schlittler ◽  
...  
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Plasma Volume ◽  
Blood Viscosity ◽  
Hypobaric Hypoxia ◽  
Volume Expansion ◽  
Hypoxic Exposure ◽  
Flow Mediated Dilation ◽  
Handgrip Exercise ◽  
Plasma Volume Expansion

Using a normoxic crossover study design, we examined the impact of hypobaric hypoxia (4 days; altitude equivalent, 3,500 m) and hemoconcentration on blood viscosity, shear stress, and endothelial function. Blood viscosity increased during the hypoxic exposure and was accompanied by elevated resting and exercising arterial shear stress. Flow-mediated dilation stimulated by reactive hyperemia and handgrip exercise was preserved throughout the hypoxic exposure. Plasma volume expansion reversed the hypoxia-associated hemoconcentration and selectively increased handgrip exercise flow-mediated dilation.

scholarly journals Evidence of sex differences in the acute impact of oscillatory shear stress on endothelial function

2019 ◽  
Vol 126 (2) ◽  
pp. 314-321 ◽  
Author(s):  
Joshua C. Tremblay ◽  
Taylor V. Stimpson ◽  
Kyra E. Pyke
Keyword(s):  
Shear Stress ◽  
Sex Differences ◽  
Shear Rate ◽  
Endothelial Function ◽  
Oscillatory Shear ◽  
Flow Mediated Dilation ◽  
Similar Stimulus ◽  
Men And Women ◽  
Oscillatory Shear Stress ◽  
The Impact

Acutely imposed oscillatory shear stress (OSS) reduces reactive hyperemia flow-mediated dilation (RH-FMD) in conduit arteries of men; however, whether a similar impairment occurs in women or with FMD in response to a controlled, sustained shear stress stimulus (SS-FMD) is unknown. The purpose of this study was to determine the impact of OSS on RH-FMD and SS-FMD in men and women. OSS was provoked in the brachial artery using a 30-min forearm cuff inflation (70 mmHg). Healthy men [ n = 16, 25 yr (SD 3)] and women [ n = 16, 21 yr (SD 2)] completed the OSS intervention twice (separate days). Brachial artery endothelial function was assessed pre- and postintervention via either RH-FMD or 6 min of handgrip SS-FMD using Duplex ultrasound. The RH-FMD stimulus was calculated as shear rate area under the curve 60 s postdeflation (SRAUC60), whereas SS-FMD shear rate was targeted to produce a similar stimulus pre- and postintervention. The OSS intervention decreased RH-FMD in both sexes [men: 6.2% (SD 3.4) to 5.2% (SD 3.0); women: 5.4% (SD 2.0) to 3.1% (SD 1.8), P < 0.001), although this was accompanied by a reduced SRAUC60. There was no significant effect of the intervention on RH-FMD with SRAUC60 as a covariate ( P = 0.310). Handgrip exercise elicited a similar stimulus before and after the intervention ( P = 0.287) in men and women ( P = 0.873). Men demonstrated blunted SS-FMD [4.8% (SD 1.9) to 3.2% (SD 1.9), P < 0.001], whereas women displayed preserved SS-FMD following the intervention [3.5% (SD 1.9) to 4.0% (SD 1.9), P = 0.061]. The lower SS-FMD in men but not women following OSS provides evidence of sex differences in the effects of OSS on conduit artery endothelial function. NEW & NOTEWORTHY Acute exposure to oscillatory shear stress induces transient endothelial dysfunction in men; however, whether women experience similar impairments is unknown. Following acutely imposed oscillatory shear stress, there was a decrease in flow-mediated dilation stimulated by a physiologically relevant sustained increase in shear stress in men but not in premenopausal women. These findings demonstrate, for the first time in humans that there are sex differences in the impact of oscillatory shear stress on endothelial function.

scholarly journals UBC-Nepal Expedition: imposed oscillatory shear stress does not further attenuate flow-mediated dilation during acute and sustained hypoxia

2018 ◽  
Vol 315 (1) ◽  
pp. H122-H131 ◽  
Author(s):  
Joshua C. Tremblay ◽  
Connor A. Howe ◽  
Philip N. Ainslie ◽  
Kyra E. Pyke
Keyword(s):  
Shear Stress ◽  
Endothelial Function ◽  
Acute Hypoxia ◽  
Reactive Hyperemia ◽  
Duplex Ultrasound ◽  
Oscillatory Shear ◽  
Flow Mediated Dilation ◽  
Oscillatory Shear Stress ◽  
Sustained Hypoxia ◽  
Experimentally Induced

Experimentally induced oscillatory shear stress (OSS) and hypoxia reduce endothelial function in humans. Acute and sustained hypoxia may cause increases in resting OSS; however, whether this influences endothelial susceptibility to further increases in OSS is unknown. Healthy lowlanders ( n = 15, 30 ± 6 yr; means ± SD) participated in three OSS interventions: two interventions at sea level [normoxia and after 20 min of normobaric hypoxia (acute hypoxia, 11% O2)] and one intervention 5–7 days after a 9-day ascent to 5,050 m (sustained hypoxia). OSS was provoked in the brachial artery using a 30-min distal cuff inflation (75 mmHg). Endothelial function was assessed before and after each intervention by reactive hyperemia flow-mediated dilation (FMD). Shear stress magnitude and patterns were obtained via Duplex ultrasound. Baseline retrograde shear stress and OSS were greater in acute hypoxia versus normoxia ( P < 0.001), and OSS was elevated in sustained hypoxia versus normoxia ( P = 0.011). The intervention further augmented OSS during each condition. Preintervention FMD was decreased by 29 ± 48% in acute hypoxia and by 25 ± 31% in sustained hypoxia compared with normoxia ( P = 0.001 and 0.026); these changes correlated with changes in baseline mean and antegrade shear stress. After the intervention, FMD decreased during normoxia (−41 ± 26%, P < 0.001) and was unaltered during acute or sustained hypoxia. Therefore, a 30-min exposure to OSS reduced FMD during normoxia, a condition with an unchallenged, healthy endothelium; however, imposed OSS did not appear to worsen endothelial function during acute or sustained hypoxia. Exposure to an altered magnitude and pattern of shear stress at baseline in hypoxia may contribute to the insensitivity to further acute augmentation of OSS. NEW & NOTEWORTHY We investigated whether the endothelium remains sensitive to experimental increases in oscillatory shear stress in acute (11% O2) and sustained (2 wk at 5,050 m) hypoxia. Hypoxia altered baseline shear stress and decreased endothelial function (flow-mediated dilation); however, exposure to experimentally induced oscillatory shear stress only impaired flow-mediated dilation in normoxia.

scholarly journals Fluctuation in shear rate, with unaltered mean shear rate, improves brachial artery flow-mediated dilation in healthy, young men

2019 ◽  
Vol 126 (6) ◽  
pp. 1687-1693 ◽  
Author(s):  
Sophie M. Holder ◽  
Ellen A. Dawson ◽  
Áine Brislane ◽  
Jonny Hisdal ◽  
Daniel J. Green ◽  
...  
Keyword(s):  
Shear Stress ◽  
Shear Rate ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Negative Pressure ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Flow Mediated Dilation ◽  
Conduit Artery ◽  
Artery Flow

Increase in mean shear stress represents an important and potent hemodynamic stimulus to improve conduit artery endothelial function in humans. No previous study has examined whether fluctuations in shear rate patterns, without altering mean shear stress, impacts conduit artery endothelial function. This study examined the hypothesis that 30-min exposure to fluctuations in shear rate patterns, in the presence of unaltered mean shear rate, improves brachial artery flow-mediated dilation. Fifteen healthy men (27.3 ± 5.0 yr) completed the study. Bilateral brachial artery flow-mediated dilation was assessed before and after unilateral exposure to 30 min of intermittent negative pressure (10 s, −40mmHg; 7 s, 0 mmHg) to induce fluctuation in shear rate, while the contralateral arm was exposed to a resting period. Negative pressure significantly increased shear rate, followed by a decrease in shear rate upon pressure release (both P < 0.001). Across the 30-min intervention, mean shear rate was not different compared with baseline ( P = 0.458). A linear mixed model revealed a significant effect of time observed for flow-mediated dilation ( P = 0.029), with exploratory post hoc analysis showing an increase in the intervention arm (∆FMD +2.0%, P = 0.008), but not in the contralateral control arm (∆FMD +0.5%, P = 0.664). However, there was no effect for arm ( P = 0.619) or interaction effect ( P = 0.096). In conclusion, we found that fluctuations in shear patterns, with unaltered mean shear, improves brachial artery flow-mediated dilation. These novel data suggest that fluctuations in shear pattern, even in the absence of altered mean shear, represent a stimulus to acute change in endothelial function in healthy individuals. NEW & NOTEWORTHY Intermittent negative pressure applied to the forearm induced significant fluctuations in antegrade and retrograde shear rate, while mean shear was preserved relative to baseline. Our exploratory study revealed that brachial artery flow-mediated dilation was significantly improved following 30-min exposure to intermittent negative pressure. Fluctuations in blood flow or shear rate, with unaltered mean shear, may have important implications for vascular health; however, further research is required to identify the underlying mechanisms and potential long-term health benefits.

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