Increased response of brachial artery diameter to norepinephrine in hypertensive patients

1988 ◽  
Vol 255 (1) ◽  
pp. H36-H43 ◽  
Author(s):  
S. Laurent ◽  
L. Juillerat ◽  
G. M. London ◽  
J. Nussberger ◽  
H. Brunner ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Vascular Reactivity ◽  
Arterial Disease ◽  
Plasma Norepinephrine ◽  
Brachial Artery Diameter ◽  
Hypertensive Patients ◽  
Small Arteries ◽  
Large Arteries ◽  
Normotensive Subjects

The hyperresponsiveness of small arteries to norepinephrine is well documented in essential hypertensive patients. Our objective was to investigate in situ the reactivity to norepinephrine of the diameter of large arteries, which are involved in the arterial disease of hypertension as well as small arteries. Brachial artery diameter, blood flow velocity, local volumic blood flow, and local vascular resistances were determined noninvasively with a pulsed Doppler system in 19 patients with essential hypertension and 9 normotensive subjects, before and after the administration of placebo (glucose) or increasing doses of norepinephrine (10, 20, and 40 ng.kg-1.min-1 iv) given in a single-blind fashion. In hypertensive patients, norepinephrine (40 ng.kg-1.min-1) induced 1) a significant decrease in brachial artery diameter, local blood velocity, volumic flow, and conductance and 2) a small increase in mean arterial pressure. These hemodynamic changes did not occur in the placebo group and were significantly greater in hypertensive patients than in normotensive subjects, although plasma norepinephrine increased to the same extent in both groups. We conclude that in hypertensive patients the increase in vascular reactivity to norepinephrine involves not only the resistive vessels but also the large arteries thus decreasing their conducting and buffering function.

Effect of acute sympathetic nervous system activation on flow-mediated dilation of brachial artery

2006 ◽  
Vol 290 (4) ◽  
pp. H1446-H1453 ◽  
Author(s):  
Kenneth S. Dyson ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Brachial Artery ◽  
Cold Pressor Test ◽  
Plasma Norepinephrine ◽  
Flow Mediated Dilation ◽  
Brachial Artery Diameter ◽  
Peak Shear Stress ◽  
Sympathetic Nervous ◽  
General Response

We tested the hypothesis that flow-mediated dilation (FMD) of the brachial artery would be impaired by acute increases in sympathetic nervous system activity (SNA) in models where similar peak shear stress stimulus was achieved by varying the duration of forearm muscle ischemia. Eleven healthy young men were studied under four different conditions, each with its own control: lower body suction (LBS), cold pressor test (CPT), mental arithmetic task (MAT), and activation of muscle chemoreflex (MCR). The duration of ischemia before observation of FMD by ultrasound imaging was 5 min each for control, LBS, and CPT; 3 min for MAT; and 2-min for MCR. Peak shear rate was not different between control and any of the SNA conditions, although total shear in the first minute was reduced in MAT. MCR was the only condition in which brachial artery vasoconstriction was observed before forearm occlusion [4.38 (SD 0.53) vs. control 4.60 (SD 0.53) mm, P < 0.05]; however, diameter increased to the same absolute value as that of the control, so the percent FMD was greater for MCR [9.85 (SD 2.33) vs. control 5.29 (SD 1.50)%]. Blunting of the FMD response occurred only in the CPT model [1.51 (SD 1.20)%]. During SNA, the increase in plasma cortisol from baseline was significant only for MCR; the increase in plasma norepinephrine was significant for MCR, LBS, and CPT; and the increase in epinephrine was significant only for MCR. These results showed that the four models employed to achieve increases in SNA had different effects on baseline brachial artery diameter and that blunted FMD is not a general response to increased SNA.

scholarly journals Measuring peripheral resistance and conduit arterial structure in humans using Doppler ultrasound

2005 ◽  
Vol 98 (6) ◽  
pp. 2311-2315 ◽  
Author(s):  
Louise H. Naylor ◽  
Cara J. Weisbrod ◽  
Gerry O'Driscoll ◽  
Daniel J. Green
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Peripheral Resistance ◽  
Artery Blood Flow ◽  
Brachial Artery Diameter ◽  
Resistance Vessel ◽  
Conduit Artery ◽  
Significant Difference ◽  
Vessel Structure

The purpose of this study was to establish valid indexes of conduit and resistance vessel structure in humans by using edge detection and wall tracking of high-resolution B-mode arterial ultrasound images, combined with synchronized Doppler waveform envelope analysis, to calculate conduit artery blood flow and diameter continuously across the cardiac cycle. Nine subjects aged 36.7 (9.2) yr underwent, on separate days, assessment of brachial artery blood flow and diameter response to 5-, 10-, and 15-min periods of forearm ischemia in the presence and absence of combined sublingual glyceryl trinitrate (GTN) administration. Two further sessions examined responses to ischemic exercise, one in combination with GTN. The peak brachial artery diameter was observed in response to the combination of ischemic exercise and GTN; a significant difference existed between resting brachial artery diameter and peak brachial artery diameter, indicating that resting diameter may be a poor measure of conduit vessel structure in vivo. Peak brachial artery flow was also observed in response to a combination of forearm ischemia exercise and GTN administration, the response being greater than that induced by periods of ischemia, GTN, or ischemic exercise alone. These data indicate that noninvasive indexes of conduit and resistance vessel structure can be simultaneously determined in vivo in response to a single, brief, stimulus and that caution should be applied in using resting arterial diameter as a surrogate measure of conduit artery structure in vivo.

Surface Stiffness of Patient-Specific Arterial Segments With Varying Plaque Compositions

2013 ◽  
Author(s):  
Craig J. Bennetts ◽  
Ahmet Erdemir ◽  
Melissa Young
Keyword(s):  
United States ◽  
Blood Flow ◽  
Peripheral Arterial Disease ◽  
Arterial Disease ◽  
The United States ◽  
Patient Specific ◽  
Large Arteries ◽  
Surface Stiffness ◽  
Peripheral Arterial

Peripheral arterial disease (PAD), resulting from the accumulation of plaque, causes obstruction of blood flow in the large arteries in the arm and leg. In the United States, approximately 8.4 million people over the age of 40 have PAD [1]. If not treated, PAD can cause ischemic ulcerations and gangrene, which could eventually lead to amputation. Approximately, 25% of patients with PAD have worsening limb symptoms over 5 years, 7% requiring revascularization, and 4% requiring amputation [2].

scholarly journals Brachial artery diameter, blood flow and flow-mediated dilation in sleep-disordered breathing

2009 ◽  
Vol 14 (4) ◽  
pp. 351-360 ◽  
Author(s):  
Hassan A Chami ◽  
Michelle J Keyes ◽  
Joseph A Vita ◽  
Gary F Mitchell ◽  
Martin G Larson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Sleep Disordered Breathing ◽  
Flow Mediated Dilation ◽  
Brachial Artery Diameter ◽  
Disordered Breathing

Occlusion cuff position is an important determinant of the time course and magnitude of human brachial artery flow-mediated dilation

2000 ◽  
Vol 99 (4) ◽  
pp. 261-267 ◽  
Author(s):  
Karen L. BERRY ◽  
R. Andrew P. SKYRME-JONES ◽  
Ian T. MEREDITH
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Time Course ◽  
Arterial Occlusion ◽  
Flow Mediated Dilation ◽  
Reactive Hyperaemia ◽  
Upper Arm ◽  
Brachial Artery Diameter ◽  
Occlusion Cuff ◽  
Forearm Occlusion

Non-invasive ultrasound techniques to assess flow-mediated vasodilation (FMD) are frequently used to assess arterial endothelial vasodilator function. However, the range of normal values varies considerably, possibly due to differences in methodological factors. We sought to determine the effect of occlusion cuff position on the time course and magnitude of brachial artery blood flow and flow-mediated dilation. Twelve healthy subjects underwent measurements of forearm blood flow using venous occlusion plethysmography (VOP) before and after 5 min of susprasystolic cuff inflation, using two randomly assigned occlusion cuff positions (upper arm and forearm). An additional 16 subjects underwent two brachial ultrasound studies, using the two cuff positions, to assess the extent and time course of changes in brachial artery diameter and blood flow. Maximum increase in blood flow (peak reactive hyperaemia), measured by VOP, occurred immediately upon each cuff deflation, but was greater after upper arm compared with forearm arterial occlusion (33.1±3.1 versus 22.8±2.2 ml/min per forearm tissue, P = 0.001). Maximal brachial artery FMD was significantly greater following upper arm occlusion (9.0±1.2%, mean±S.E.M.) compared with forearm occlusion (5.9±0.7%, P = 0.01). The time course of the change in brachial artery diameter was affected differently in response to each protocol. The time to peak dilation following upper arm occlusion was delayed by 22 s compared with forearm occlusion. Occlusion cuff position is thus a powerful determinant of peak reactive hyperaemia, volume repaid and the extent and time course of brachial artery FMD. Positioning the cuff on the upper arm produces a greater FMD. These results highlight the need for comparisons between FMD studies to be made with care.

scholarly journals GLP-1 and Insulin Recruit Muscle Microvasculature and Dilate Conduit Artery Individually But Not Additively in Healthy Humans

2018 ◽  
Vol 2 (2) ◽  
pp. 190-206 ◽  
Author(s):  
Alvin W K Tan ◽  
Sharmila C Subaran ◽  
Matthew A Sauder ◽  
Weidong Chai ◽  
Linda A Jahn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Muscle ◽  
Flow Velocity ◽  
Surface Area ◽  
Brachial Artery ◽  
Microvascular Perfusion ◽  
Brachial Artery Diameter ◽  
Nutrient Delivery ◽  
Conduit Artery ◽  
Endothelial Surface

Abstract Context Glucagon-like peptide-1 (GLP-1) and insulin increase muscle microvascular perfusion, thereby increasing tissue endothelial surface area and nutrient delivery. Objective To examine whether GLP-1 and insulin act additively on skeletal and cardiac microvasculature and conduit artery. Design Healthy adults underwent three study protocols in random order. Setting Clinical Research Unit at the University of Virginia. Methods Overnight-fasted participants received an intravenous infusion of GLP-1 (1.2 pmol/kg/min) or normal saline for 150 minutes with or without a 2-hour euglycemic insulin clamp (1 mU/kg/min) superimposed from 30 minutes onward. Skeletal and cardiac muscle microvascular blood volume (MBV), flow velocity, and flow; brachial artery diameter, flow velocity, and blood flow; and pulse wave velocity (PWV) were measured. Results GLP-1 significantly increased skeletal and cardiac muscle MBV and microvascular blood flow (MBF) after 30 minutes; these remained elevated at 150 minutes. Insulin also increased skeletal and cardiac muscle MBV and MBF. Addition of insulin to GLP-1 did not further increase skeletal and cardiac muscle MBV and MBF. GLP-1 and insulin increased brachial artery diameter and blood flow, but this effect was not additive. Neither GLP-1, insulin, nor GLP-1 and insulin altered PWV. Combined GLP-1 and insulin infusion did not result in higher whole-body glucose disposal. Conclusion GLP-1 and insulin at physiological concentrations acutely increase skeletal and cardiac muscle microvascular perfusion and dilate conduit artery in healthy adults; these effects are not additive. Thus, GLP-1 and insulin may regulate skeletal and cardiac muscle endothelial surface area and nutrient delivery under physiological conditions.

scholarly journals Noninvasive Assessment of Endothelium-Dependent Flow-Mediated Dilation of the Brachial Artery

1997 ◽  
Vol 2 (2) ◽  
pp. 87-92 ◽  
Author(s):  
Akimi Uehata ◽  
Eric H Lieberman ◽  
Marie D Gerhard ◽  
Todd J Anderson ◽  
Peter Ganz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Vascular Function ◽  
Reactive Hyperemia ◽  
Intraobserver Variability ◽  
Flow Mediated Dilation ◽  
Noninvasive Technique ◽  
Brachial Artery Diameter ◽  
Cuff Occlusion

Coronary atherosclerosis is characterized by an early loss of endothelium-dependent vasodilation. However, the methods of assessing coronary endothelial function are invasive and difficult to repeat over time. Recently, a noninvasive ultrasound method has been widely used to measure flow-mediated dilation in the brachial artery as a surrogate test for endothelial function. We seek to further validate this method of measuring vascular function. The brachial artery diameters and blood flow of 20 normal volunteers (10 males and 10 females) were measured using high resolution (7.5 MHz) ultrasound and strain gauge plethysmography. Flow-mediated endothelium-dependent vasodilation was measured in the brachial artery during reactive hyperemia after 5 minutes of cuff occlusion in the upper arm. The brachial artery diameter increased maximally by 9.7 ± 4.3% from baseline at 1 min after cuff release and blood flow increased by 1002 ± 376%. Five min of cuff occlusion was sufficient to achieve 97 ± 6% of maximal brachial artery dilation and degree of dilation was not different whether the cuff was inflated proximally or distally to the image site. The intraobserver variability in measuring brachial diameters was 2.9 % and the variability of the hyperemic response was 1.4%. In young, healthy men and women, the baseline brachial artery diameter was the only factor that was predictive of the flow-mediated vasodilation response. The brachial noninvasive technique has been further validated by the determination of flow-mediated dilation. This method of assessing endothelial function may help to determine the importance of vasodilator dysfunction as a risk factor in the development of atherosclerosis.

scholarly journals Rarefaction and blood pressure in systemic and pulmonary arteries

2012 ◽  
Vol 705 ◽  
pp. 280-305 ◽  
Author(s):  
Mette S. Olufsen ◽  
N. A. Hill ◽  
Gareth D. A. Vaughan ◽  
Christopher Sainsbury ◽  
Martin Johnson
Keyword(s):  
Blood Flow ◽  
Theoretical Calculations ◽  
Pulmonary Arteries ◽  
Cross Sectional ◽  
Small Arteries ◽  
Large Arteries ◽  
Vascular Bed ◽  
Vascular Beds ◽  
The Impact ◽  
Averaged Model

AbstractThe effects of vascular rarefaction (the loss of small arteries) on the circulation of blood are studied using a multiscale mathematical model that can predict blood flow and pressure in the systemic and pulmonary arteries. We augmented a model originally developed for the systemic arteries by Olufsen and coworkers and Ottesen et al. (2004) to (a) predict flow and pressure in the pulmonary arteries, and (b) predict pressure propagation along the small arteries in the vascular beds. The systemic and pulmonary arteries are modelled as separate bifurcating trees of compliant and tapering vessels. Each tree is divided into two parts representing the ‘large’ and ‘small’ arteries. Blood flow and pressure in the large arteries are predicted using a nonlinear cross-sectional-area-averaged model for a Newtonian fluid in an elastic tube with inflow obtained from magnetic resonance measurements. Each terminal vessel within the network of the large arteries is coupled to a vascular bed of small ‘resistance’ arteries, which are modelled as asymmetric structured trees with specified area and asymmetry ratios between the parent and daughter arteries. For the systemic circulation, each structured tree represents a specific vascular bed corresponding to major organs and limbs. For the pulmonary circulation, there are four vascular beds supplied by the interlobar arteries. This paper presents the first theoretical calculations of the propagation of the pressure and flow waves along systemic and pulmonary large and small arteries. Results for all networks are in agreement with published observations. Two studies were done with this model. First, we showed how rarefaction can be modelled by pruning the tree of arteries in the microvascular system. This was done by modulating parameters used for designing the structured trees. Results showed that rarefaction leads to increased mean and decreased pulse pressure in the large arteries. Second, we investigated the impact of decreasing vessel compliance in both large and small arteries. Results showed that the effects of decreased compliance in the large arteries far outweigh the effects observed when decreasing the compliance of the small arteries. We further showed that a decrease of compliance in the large arteries results in pressure increases consistent with observations of isolated systolic hypertension, as occurs in ageing.

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