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.

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.

Effect of cardiac pacing on forearm vascular responses and nitric oxide function

2002 ◽  
Vol 283 (4) ◽  
pp. H1354-H1360 ◽  
Author(s):  
Daniel Green ◽  
Craig Cheetham ◽  
Chelsea Henderson ◽  
Rukshen Weerasooriya ◽  
Gerard O'Driscoll
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Blood Flow ◽  
Brachial Artery ◽  
Pulse Pressure ◽  
Forearm Blood Flow ◽  
Cardiac Pacing ◽  
Pulse Frequency ◽  
Brachial Artery Diameter

We examined the hypothesis that changes in heart rate at rest influence bioactivity of nitric oxide (NO) in humans by examining forearm blood flow responses during cardiac pacing in six subjects. Peak forearm and mean forearm blood flows across the cardiac cycle were continuously recorded at baseline and during pacing, with the use of high-resolution brachial artery ultrasound and Doppler flow velocity measurement. The brachial artery was cannulated to allow continuous infusion of saline or N G-monomethyl-l-arginine (l-NMMA). As heart rate increased, no changes in pulse pressure and mean or peak blood flow were evident. l-NMMA had no effect on brachial artery diameter, velocity, or flows compared with saline infusion. These results contrast with our recent findings that exercise involving the lower body, associated with increases in heart rate and pulse pressure, also increased forearm blood flow, the latter response being diminished by l-NMMA. These data suggest that changes in blood pressure, rather than pulse frequency, may be the stimulus for shear stress-mediated NO release in vivo.

scholarly journals Exercise-induced brachial artery blood flow and vascular function is impaired in systemic sclerosis

2016 ◽  
Vol 311 (6) ◽  
pp. H1375-H1381 ◽  
Author(s):  
Daniel R. Machin ◽  
Heather L. Clifton ◽  
Ryan S. Garten ◽  
Jayson R. Gifford ◽  
Russell S. Richardson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Systemic Sclerosis ◽  
Brachial Artery ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Artery Blood Flow ◽  
Handgrip Exercise ◽  
Brachial Artery Diameter ◽  
Exercise Induced

Systemic sclerosis (SSc) is a rare autoimmune disease characterized by debilitating fibrosis and vascular dysfunction; however, little is known about the circulatory response to exercise in this population. Therefore, we examined the peripheral hemodynamic and vasodilatory responses to handgrip exercise in 10 patients with SSc (61 ± 4 yr) and 15 age-matched healthy controls (56 ± 5 yr). Brachial artery diameter, blood flow, and mean arterial pressure (MAP) were determined at rest and during progressive static-intermittent handgrip exercise. Patients with SSc and controls were similar in body stature, handgrip strength, and MAP; however, brachial artery blood flow at rest was nearly twofold lower in patients with SSc compared with controls (22 ± 4 vs. 42 ± 5 ml/min, respectively; P < 0.05). Additionally, SSc patients had an ∼18% smaller brachial artery lumen diameter with an ∼28% thicker arterial wall at rest ( P < 0.05). Although, during handgrip exercise, there were no differences in MAP between the groups, exercise-induced hyperemia and therefore vascular conductance were ∼35% lower at all exercise workloads in patients with SSc ( P < 0.05). Brachial artery vasodilation, as assessed by the relationship between Δbrachial artery diameter and Δshear rate, was significantly attenuated in the patients with SSc ( P < 0.05). Finally, vascular dysfunction in the patients with SSc was accompanied by elevated blood markers of oxidative stress and attenuated endogenous antioxidant activity ( P < 0.05). Together, these findings reveal attenuated exercise-induced brachial artery blood flow and conduit arterial vasodilatory dysfunction during handgrip exercise in SSc and suggest that elevated oxidative stress may play a role.

Brachial artery modifications to blood flow-restricted handgrip training and detraining

2012 ◽  
Vol 112 (6) ◽  
pp. 956-961 ◽  
Author(s):  
Julie E. A. Hunt ◽  
Lucy A. Walton ◽  
Richard A. Ferguson
Keyword(s):  
Blood Flow ◽  
Brachial Artery ◽  
Load Resistance ◽  
Muscle Size ◽  
Brachial Artery Diameter ◽  
Conduit Artery ◽  
Flow Restriction ◽  
Maximal Diameter ◽  
Low Load ◽  
Occlusion Cuff

Low load resistance training with blood flow restriction (BFR) can increase muscle size and strength, but the implications on the conduit artery are uncertain. We examined the effects of low-load dynamic handgrip training with and without BFR, and detraining, on measures of brachial artery function and structure. Nine male participants (26 ± 4 yr, 178 ± 3 cm, 78 ± 10 kg) completed 4 wk (3 days/wk) of dynamic handgrip training at 40% 1 repetition maximum (1RM). In a counterbalanced manner, one forearm trained under BFR (occlusion cuff at 80 mmHg) and the other under nonrestricted (CON) conditions. Brachial artery function [flow-mediated dilation (FMD)] and structure (diameter) were assessed using Doppler ultrasound. Measurements were made before training (pretraining), after training (posttraining), and after 2-wk no training (detraining). Brachial artery diameter at rest, in response to 5-min ischemia (peak diameter), and ischemic exercise (maximal diameter) increased by 3.0%, 2.4%, and 3.1%, respectively, after BFR training but not after CON. FMD did not change at any time point in either arm. Vascular measures in the BFR arm returned to baseline after 2 wk detraining with no change after CON. The data demonstrate that dynamic low-load handgrip training with BFR induced transient adaptations to conduit artery structure but not function.

scholarly journals Glucose-dependent blood flow dynamics in murine pancreatic islets in vivo

2010 ◽  
Vol 298 (4) ◽  
pp. E807-E814 ◽  
Author(s):  
Lara R. Nyman ◽  
Eric Ford ◽  
Alvin C. Powers ◽  
David W. Piston
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Pancreatic Islets ◽  
Fluorescent Protein ◽  
Yellow Fluorescent Protein ◽  
Cell Types ◽  
Β Cells ◽  
Islet Blood Flow ◽  
Significant Difference

Pancreatic islets are highly vascularized and arranged so that regions containing β-cells are distinct from those containing other cell types. Although islet blood flow has been studied extensively, little is known about the dynamics of islet blood flow during hypoglycemia or hyperglycemia. To investigate changes in islet blood flow as a function of blood glucose level, we clamped blood glucose sequentially at hyperglycemic (∼300 mg/dl or 16.8 mM) and hypoglycemic (∼50 mg/dl or 2.8 mM) levels while simultaneously imaging intraislet blood flow in mouse models that express green fluorescent protein in the β-cells or yellow fluorescent protein in the α-cells. Using line scanning confocal microscopy, in vivo blood flow was assayed after intravenous injection of fluorescent dextran or sulforhodamine-labeled red blood cells. Regardless of the sequence of hypoglycemia and hyperglycemia, islet blood flow is faster during hyperglycemia, and apparent blood volume is greater during hyperglycemia than during hypoglycemia. However, there is no change in the order of perfusion of different islet endocrine cell types in hypoglycemia compared with hyperglycemia, with the islet core of β-cells usually perfused first. In contrast to the results in islets, there was no significant difference in flow rate in the exocrine pancreas during hyperglycemia compared with hypoglycemia. These results indicate that glucose differentially regulates blood flow in the pancreatic islet vasculature independently of blood flow in the rest of the pancreas.

Normal pregnancy is associated with enhanced endothelium-dependent flow-mediated vasodilation

1999 ◽  
Vol 276 (3) ◽  
pp. H821-H825 ◽  
Author(s):  
Inge Dørup ◽  
Kristjar Skajaa ◽  
Keld E. Sørensen
Keyword(s):  
Brachial Artery ◽  
Reactive Hyperemia ◽  
Peripheral Resistance ◽  
First Trimester ◽  
Normal Pregnancy ◽  
Brachial Artery Diameter ◽  
Vasomotor Function ◽  
Pregnancy Status ◽  
Dependent Flow ◽  
Flow Mediated Vasodilation

Normal pregnancy is characterized by reduced systemic vascular resistance, which may be mediated by nitric oxide (NO). We compared endothelial vasomotor function in 71 normal pregnant women (13 in first, 29 in middle, and 29 in last trimester) to 37 healthy age-matched controls. With external ultrasound, brachial artery diameter was measured at rest, during reactive hyperemia [with increased flow causing endothelium-dependent dilation (FMD)], and after sublingual nitroglycerin (causing endothelium-independent dilation). Compared with controls, resting flow and brachial artery diameter were significantly higher during the middle and last trimesters. Reactive hyperemia was reduced in all pregnant groups. FMD increased from the first trimester (by 26%), reaching the highest value in the last trimester (to 47% above nonpregnant values). FMD was significantly correlated to pregnancy status (nonpregnant or pregnant) and to vessel size. Nitroglycerin-induced dilation was similar in pregnant and nonpregnant women. A longitudinal study of eight women evaluated in the first, middle, and last trimesters confirmed an increase in FMD throughout pregnancy. The study supports the idea that basal and stimulated NO activity is enhanced in normal pregnancy and may contribute to the decrease in peripheral resistance.

Repeated increases in blood flow, independent of exercise, enhance conduit artery vasodilator function in humans

2011 ◽  
Vol 300 (2) ◽  
pp. H664-H669 ◽  
Author(s):  
Louise H. Naylor ◽  
Howard Carter ◽  
Matthew G. FitzSimons ◽  
N. Timothy Cable ◽  
Dick H. J. Thijssen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Complex Stimulus ◽  
Artery Blood Flow ◽  
Handgrip Exercise ◽  
Repeated Heating ◽  
Conduit Artery ◽  
Pressure Cuff ◽  
Ischemic Handgrip Exercise ◽  
Bilateral Heating

This study aimed to determine the importance of repeated increases in blood flow to conduit artery adaptation, using an exercise-independent repeated episodic stimulus. Recent studies suggest that exercise training improves vasodilator function of conduit arteries via shear stress-mediated mechanisms. However, exercise is a complex stimulus that may induce shear-independent adaptations. Nine healthy men immersed their forearms in water at 42°C for three 30-min sessions/wk across 8 wk. During each session, a pneumatic pressure cuff was inflated around one forearm to unilaterally modulate heating-induced increases in shear. Forearm heating was associated with an increase in brachial artery blood flow ( P < 0.001) and shear rate ( P < 0.001) in the uncuffed forearm; this response was attenuated in the cuffed limb ( P < 0.005). Repeated episodic exposure to bilateral heating induced an increase in endothelium-dependent vasodilation in response to 5-min ischemic ( P < 0.05) and ischemic handgrip exercise ( P < 0.005) stimuli in the uncuffed forearm, whereas the 8-wk heating intervention did not influence dilation to either stimulus in the cuffed limb. Endothelium-independent glyceryl trinitrate responses were not altered in either limb. Repeated heating increases blood flow to levels that enhance endothelium-mediated vasodilator function in humans. These findings reinforce the importance of the direct impacts of shear stress on the vascular endothelium in humans.

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