Reproducibility of blood flow and post-occlusive reactive hyperaemia as measured by venous occlusion plethysmography

Thijssen, Dick H. J.; Bleeker, Michiel W. P.; Smits, Paul; Hopman, Maria T. E.

doi:10.1042/cs20040177

Cited by 70 publications

(74 citation statements)

References 42 publications

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“…Leg blood flow (in ml/min per dl of leg tissue) was calculated as the slope of the volume change curve over a 4-second interval, starting directly after the inflation-induced cuff artifact (2 seconds). 21 Thigh vascular resistance was calculated as the mean arterial pressure (mm Hg) divided by thigh blood flow (in ml/min/dL) and expressed in arbitrary units (AU; mm Hg/mL/min/dL). Because of the differences in baseline vascular characteristics between SCI and control subjects, analysis of absolute values could affect the comparison between both groups.…”

Section: Discussionmentioning

confidence: 99%

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A Causal Role for Endothelin-1 in the Vascular Adaptation to Skeletal Muscle Deconditioning in Spinal Cord injury

Thijssen

Ellenkamp

Kooijman

et al. 2007

ATVB

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Objective-Endothelin-1 (ET-1) contributes to the increased peripheral resistance in heart failure and hypertension.Physical inactivity is associated with cardiovascular disease and characterized by increased vascular tone. In this study, we assess the contribution of ET-1 to the increased vascular tone in the extremely deconditioned legs of spinal cord-injured (SCI) individuals before and after exercise training. Methods and Results-In 8 controls and 8 SCI individuals, bilateral thigh blood flow was measured by plethysmography before and during the administration of an ET A /ET B -receptor blocker into the femoral artery. In SCI, this procedure was repeated after 6 weeks of electro-stimulated training. In a subset of SCI (nϭ4), selective ET A -receptor blockade was performed to determine the role of the ET A -receptors. In controls, dual ET-receptor blockade increased leg blood flow at the infused side (10%, PϽ0.05), indicating a small contribution of ET-1 to leg vascular tone. In SCI, baseline blood flow was lower compared with controls (Pϭ0.05). In SCI, dual ET-receptor blockade increased blood flow (41%, PϽ0.001). This vasodilator response was significantly larger in SCI compared with controls (PϽ0.001). The response to selective ET A -receptor blockade was similar to the effect of dual blockade. Electro-stimulated training normalized baseline blood flow in SCI and reduced the response to dual ET-receptor blockade in the infused leg (29%, Pϭ0.04). Key Words: endothelin receptor Ⅲ endothelium Ⅲ exercise Ⅲ cardiovascular disease Ⅲ paraplegia T he endothelium plays an important role in the regulation of vascular tone via the release of vasodilator and vasoconstrictor substances. Endothelin-1 (ET-1) 1 is one of the most potent endothelium-derived constricting factors, and contributes to the regulation of peripheral vascular tone 2,3 by interacting with ET A -4 and ET B -receptors 5 on smooth muscle and endothelial cells. 6,7 In several pathological conditions, such as pulmonary 8 and systemic essential hypertension, 9 heart failure, 10,11 atherosclerosis, and obesity, 12 ET-1 plasma levels are elevated and contribute to the increased vascular tone observed in these disease states. In models of skeletal muscle deconditioning, such as unilateral limb suspension 13 and bed rest, 14 vascular tone is also increased. In the present study, we hypothesize that the elevated vascular tone in deconditioned muscles can be explained by an augmented contribution of ET-1. Conclusion-ET-1 mediates the increased vascular tone of extremely inactive legs of SCI individuals by increased activation of ETIndividuals with a spinal cord injury offer a unique model of nature to assess peripheral vascular adaptations to inactivity because the skeletal muscles below the level of the lesion are paralyzed and, therefore, extremely inactive. Previous research demonstrated that extensive vascular adaptations, such as an increased leg vascular tone, occur in the inactive and paralyzed legs of spinal cord-injured individuals. 15 These adaptation...

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Section: Discussionmentioning

confidence: 99%

“…20 A mercury-in-silastic strain gauge (Hokanson Inc) was placed at mid-thigh, at least 10 cm above the patella and at least 4 cm below the cuff. 21 The lower legs were supported Ϸ10 cm above heart level to facilitate venous outflow between the venous occlusion periods.…”

Section: Protocolmentioning

confidence: 99%

A Causal Role for Endothelin-1 in the Vascular Adaptation to Skeletal Muscle Deconditioning in Spinal Cord injury

Thijssen

Ellenkamp

Kooijman

et al. 2007

ATVB

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“…We have previously shown that the reproducibility of upper leg blood flow measurements is good (Thijssen et al 2005a). The thigh cuffs were simultaneously inflated to 50 mmHg using a rapid cuff inflator (Hokanson E-20, D.E.…”

Section: Methodsmentioning

confidence: 99%

Preserved contribution of nitric oxide to baseline vascular tone in deconditioned human skeletal muscle

Bleeker¹,

Kooijman

Rongen

et al. 2005

The Journal of Physiology

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Deconditioning is a risk factor for cardiovascular disease. Exercise reduces this risk, possibly by improving the vascular endothelial nitric oxide (NO) pathway. The effect of deconditioning on the NO pathway is largely unknown. This study was designed to assess baseline NO availability in the leg vascular bed after extreme, long-term deconditioning (spinal cord-injured individuals, SCI) as well as after moderate, short-term deconditioning (4 weeks of unilateral lower limb suspension, ULLS). For this purpose, seven SCI were compared with seven matched controls. Additionally, seven healthy subjects were studied pre-and post-ULLS. Leg blood flow was measured by venous occlusion plethysmography at baseline and during infusion of 5 incremental dosages of N G -monomethyl-L-arginine (L-NMMA) into the femoral artery. Sodium nitroprusside (SNP) was infused to test vascular responsiveness to NO. Baseline leg vascular resistance tended to be higher in SCI compared with controls (37 ± 4 versus 31 ± 2 arbitrary units (AU), P = 0.06). Deconditioning altered neither the vasoconstrictor response to L-NMMA (increase in resistance in SCI versus controls: 102 ± 33% versus 69 ± 9%; pre-versus post-ULLS: 95 ± 18% versus 119 ± 15%), nor the vascular responsiveness to NO. In conclusion, two human in vivo models of deconditioning show a preserved baseline NO availability in the leg skeletal muscle vascular bed.

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“…Coefficient of variation was calculated for the FMD% responses in the noncuffed arm for each intervention day. 26 …”

Section: Statisticsmentioning

confidence: 99%

Retrograde Flow and Shear Rate Acutely Impair Endothelial Function in Humans

Thijssen

Dawson

Tinken³

et al. 2009

Hypertension

254

296

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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 (24Ϯ3 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 (PϽ0.001). 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 (PϽ0.05). The decrease in flow-mediated dilation after the 75-mm Hg intervention was significantly larger than that observed after a 50-mm Hg intervention (Pϭ0.03). 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. More recent studies indicate that changes in shear stress on the endothelial cell membrane are a key stimulus for adaptation in both vascular function and remodeling. 2-6 Elevation in endothelial shear stress, such as that present during exercise, is a key stimulus to express antiatherogenic genes (eg, endothelial NO synthase) 7 and decrease proatherogenic genes (eg, endothelin 1). 8 Importantly, these changes in gene expression are associated with enhanced endothelial function in vivo. 9,10 Although changes in shear can clearly transduce beneficial arterial adaptations, it is also apparent from studies performed in vitro and in animals that oscillatory shear stress, characterized by high levels of retrograde shear, can increase the expression of proatherogenic, and decreases antiatherogenic, genes. 11 For example, oscillatory shear increases endothelin 1 expression 12 and adhesion molecules 13,14 and enhances the release of superoxide 15 and expression of reactive oxygen species-producing enzymes (ie, NADPH oxidase) 16,17 but decreases endothelial NO synthase expression. 16,17 However, the impact of changing retrograde shear stress has never been examined in humans.The primary purpose of this study was to examine the impact of different magnitudes of retrograde shear stress on endothelial function in humans. To this end, we simultaneously examined brachial artery endothelial function in both arms of healthy subjects before and after 30-minute exposure to stepwise increases in retrograde shear induced by cuff inflation on 1 forearm to 25, 50, or 75 mm Hg. In this wa...

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Reproducibility of blood flow and post-occlusive reactive hyperaemia as measured by venous occlusion plethysmography

Cited by 70 publications

References 42 publications

A Causal Role for Endothelin-1 in the Vascular Adaptation to Skeletal Muscle Deconditioning in Spinal Cord injury

A Causal Role for Endothelin-1 in the Vascular Adaptation to Skeletal Muscle Deconditioning in Spinal Cord injury

Preserved contribution of nitric oxide to baseline vascular tone in deconditioned human skeletal muscle

Retrograde Flow and Shear Rate Acutely Impair Endothelial Function in Humans

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