Effects of Ischemic Reperfusion Injury and Remote Conditioning on Passive Leg Raising-Induced Brachial-Artery Dilation

Cardiology ◽  
2016 ◽  
Vol 134 (3) ◽  
pp. 320-324
Author(s):  
Manasi Bapat ◽  
Bhawna Sharma ◽  
Andrew Persits ◽  
Hue Van Le ◽  
Jack Janani ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Brachial Artery ◽  
Passive Leg Raising ◽  
Ischemic Conditioning ◽  
Ischemic Reperfusion ◽  
Before And After ◽  
Vasodilator Reserve ◽  
Remote Conditioning ◽  
Conditioning Stimuli ◽  
Healthy Males

Objectives: Passive leg raising (PLR) has been proposed to assess arterial vasodilator reserve and possibly endothelial function. Since endothelial function is sensitive to ischemic-reperfusion (I-R) injury, we determined the effects of I-R injury and ischemic conditioning on PLR-induced brachial-artery dilation (BAD), i.e. PLR-BAD. Methods: We induced PLR-BAD before and after ipsilateral arm I-R injury (7.5 min of occlusion) in 20 healthy males aged 29 ± 6 years. The protocol was repeated in combination with remote conditioning stimuli (3 × 30 s of contralateral arm occlusions). Results: PLR resulted in significant BAD (3.85%, p < 0.001) before but not after prolonged ischemia (0.25%, p = 0.38). I-R injury, along with either preischemic or postischemic conditioning restored the PLR-BAD response (before: 3.11%, p < 0.001 and after: 3.74%, p < 0.001). Conclusions: I-R injury blunts the BAD induced by PLR. Remote pre- and postconditioning restore this response. These findings are similar to those previously reported using hyperemia and ultrasound to assess BAD.

Retrograde shear rate in formerly preeclamptic and healthy women before and after exercise training: relationship with endothelial function

2014 ◽  
Vol 307 (3) ◽  
pp. H418-H425 ◽  
Author(s):  
Ralph R. Scholten ◽  
Marc E. A. Spaanderman ◽  
Daniel J. Green ◽  
Maria T. E. Hopman ◽  
Dick H. J. Thijssen
Keyword(s):  
Shear Rate ◽  
Exercise Training ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Low Frequency ◽  
Power Spectral Analysis ◽  
Aerobic Exercise Training ◽  
Before And After ◽  
The Impact ◽  
Retrograde Shear

Blood flow patterns in conduit arteries characterized by high levels of retrograde shear stress can be detrimental for vascular health. In this study we examined whether retrograde shear rate and endothelial function are related in healthy and formerly preeclamptic (PE) women and whether this relationship is altered by exercise training. Formerly PE women (32 ± 4 yr, n = 20) and controls (32 ± 4 yr, n = 20), all 6–12 mo postpartum, performed 12-wk aerobic exercise training. We measured brachial artery shear rate (SR) and endothelial function by flow-mediated dilation (FMD, echo-Doppler). We additionally performed power spectral analysis of heart rate variability and calculated low-frequency/high-frequency (LF/HF) ratio. Antegrade SR was not different between groups, while retrograde SR was significantly higher and FMD% lower in PE women compared with controls (both P < 0.05). Retrograde shear correlated strongly with FMD% in PE women and controls ( P < 0.05). LF/HF ratio inversely correlated with brachial artery retrograde SR and FMD% (both P < 0.05) in PE women and controls. Exercise training reduced retrograde shear, improved FMD%, and reduced LF/HF ratios similarly in both groups (all P < 0.05). Training-induced changes in retrograde SR correlated with changes in FMD% and LF/HF ratio. A higher brachial artery retrograde SR relates to lower brachial artery endothelial function, in both controls and formerly PE women. Exercise training improves retrograde SR, while the magnitude of this change correlated strongly with improvements in FMD and reductions in LF/HF ratio. Therefore, the impact of PE and exercise training on endothelial health may, at least partly, be related to retrograde shear rate.

scholarly journals Metformin Improves Skeletal Muscle Microvascular Insulin Resistance in Metabolic Syndrome

2021 ◽  
Author(s):  
Linda A Jahn ◽  
Lee M Hartline ◽  
Zhenqi Liu ◽  
Eugene J Barrett
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Pulse Wave ◽  
Metabolic Effects ◽  
Large Artery ◽  
Metformin Treatment ◽  
Radial Pulse ◽  
Before And After

Aims: Microvascular insulin resistance is present in metabolic syndrome and may contribute to increased cardiovascular disease risk and the impaired metabolic response to insulin observed. Metformin improves metabolic insulin resistance in humans. Its effects on macro and microvascular insulin resistance has not been defined. Methods: Eleven non-diabetic, metabolic syndrome subjects were studied four times (before and after 12 weeks treatment with placebo or metformin) using a crossover design, with an eight week washout interval between treatments. On each occasion, we measured three indices of large artery function (pulse wave velocity-PWV, radial pulse wave separation analysis (PWSA), brachial artery endothelial function (flow-mediated dilation-FMD) as well as muscle microvascular perfusion (contrast-enhanced ultrasound-CEU) before and 120 min into a 150 min, 1 mU/min/kg euglycemic insulin clamp. RESULTS: Metformin decreased body mass index (BMI), fat weight, and % body fat (P<0.05, each), placebo had no effect. Metformin (not placebo) improved metabolic insulin sensitivity, (clamp glucose infusion rate, P<0.01). PWV, and FMD after insulin were unaffected by metformin treatment. PWSA improved with insulin only after metformin P<0.01). Insulin decreased muscle microvascular blood volume measured by contrast ultrasound both before and after placebo and before metformin (P<0.02 for each) but not after metformin. CONCLUSIONS: Short-term metformin treatment improves both metabolic and muscle microvascular response to insulin. Metformin's effect on microvascular insulin responsiveness may contribute to its beneficial metabolic effects. Metformin did not improve aortic stiffness or brachial artery endothelial function, but enhaced radial pulse wave properties consistent with relaxation of smaller arterioles.

Passive leg raising induced brachial artery dilation: Is an old technique a simpler method to measure endothelial function?

2010 ◽  
Vol 212 (1) ◽  
pp. 188-192 ◽  
Author(s):  
Haroon Kamran ◽  
Louis Salciccioli ◽  
Vinod Namana ◽  
Bhuvaneshwari Venkatesan ◽  
Casey Santana ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Brachial Artery ◽  
Passive Leg Raising ◽  
Simpler Method

Flow-mediated dilatation following wrist and upper arm occlusion in humans: the contribution of nitric oxide

2001 ◽  
Vol 101 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Sagar N. DOSHI ◽  
Katerina K. NAKA ◽  
Nicola PAYNE ◽  
Christopher J.H. JONES ◽  
Moira ASHTON ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Function ◽  
Brachial Artery ◽  
Peak Flow ◽  
Ultrasound Probe ◽  
Upper Arm ◽  
Flow Mediated Dilatation ◽  
Synthase Inhibitor ◽  
Increased Blood Flow ◽  
Similar Peak

Flow-mediated dilatation (FMD) of the brachial artery assessed by high-resolution ultrasound is widely used to measure endothelial function. However, the technique is not standardized, with different groups using occlusion of either the wrist or the upper arm to induce increased blood flow. The validity of the test as a marker of endothelial function rests on the assumption that the dilatation observed is endothelium-dependent and mediated by nitric oxide (NO). We sought to compare the NO component of brachial artery dilatation observed following wrist or upper arm occlusion. Dilatation was assessed before and during intra-arterial infusion of the NO synthase inhibitor NG-monomethyl-l-arginine (l-NMMA) following occlusion of (i) the wrist (distal to ultrasound probe) and (ii) the upper arm (proximal to ultrasound probe) for 5min in ten healthy males. Dilatation was significantly greater after upper arm occlusion (upper arm, 11.62±3.17%; wrist, 7.25±2.49%; P = 0.003). During l-NMMA infusion, dilatation after wrist occlusion was abolished (from 7.25±2.49% to 0.16±2.24%; P < 0.001), whereas dilatation after upper arm occlusion was only partially attenuated (from 11.62±3.17% to 7.51±2.34%; P = 0.006). The peak flow stimulus was similar after wrist and upper arm occlusion. We conclude that dilatation following upper arm occlusion is greater than that observed after wrist occlusion, despite a similar peak flow stimulus. l-NMMA infusion revealed that FMD following wrist occlusion is mediated exclusively by NO, while dilatation following upper arm occlusion comprises a substantial component not mediated by NO, most probably related to tissue ischaemia around the brachial artery. FMD following wrist occlusion may be a more valid marker of endothelial function than dilatation following upper arm occlusion.

Determinants of short-term variation in arterial flow-mediated dilatation in healthy young men

2006 ◽  
Vol 110 (4) ◽  
pp. 475-482 ◽  
Author(s):  
Mikko J. Järvisalo ◽  
Laura Jartti ◽  
Jukka Marniemi ◽  
Tapani Rönnemaa ◽  
Jorma S. A. Viikari ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Brachial Artery ◽  
Serum Insulin ◽  
Circadian Variation ◽  
Low Fat ◽  
Ultrasound Technique ◽  
Brachial Artery Diameter ◽  
Flow Mediated Dilatation ◽  
Hourly Variation ◽  
Fat Meal

Brachial artery FMD (flow-mediated dilatation) is widely used as a marker of systemic arterial endothelial function. FMD, however, shows considerable 25% day-to-day variation that hinders its clinical use. The reasons for this variability are poorly characterized. Therefore the present study was designed to clarify factors responsible for the hourly variation in endothelial function, including consuming a low-fat meal and circadian rhythms in endogenous hormonal levels. Brachial artery FMD, along with serum glucose, triacylglycerols (triglycerides) and levels of several hormones were measured six times per day on two separate days 1 week apart. On one day, the subjects (healthy males: n=12, mean age, 24 years) ate a light breakfast and a standardized lunch (23.5% fat, 48.7% carbohydrate and 27.8% protein). On the other day, they had a similar breakfast after which they fasted. Postprandial FMD values (both after breakfast and after lunch) were similar to baseline FMD. FMD showed a 28% hourly variation and 27% weekly variation. Variation in plasma levels of insulin (P=0.02) associated negatively and DHPG (3,4-dihydroxyphenylglycol) (P=0.001), a marker of sympathetic nervous activation, associated positively with variation in FMD. The effects of DHPG and insulin on FMD were independent of changes in baseline brachial artery diameter, although DHPG was also inversely associated with baseline diameter. Eating a regular low-fat meal does not have any measurable effects on brachial artery endothelial function. These data suggest that strict requirements for fasting conditions may be unnecessary when measuring peripheral endothelial function using the ultrasound technique. Circadian variation in serum insulin and sympathetic tone are physiological determinants of endothelial function.

scholarly journals Influence of long-term treatment with glyceryl trinitrate on remote ischemic conditioning

2018 ◽  
Vol 315 (1) ◽  
pp. H150-H158 ◽  
Author(s):  
Marie Hauerslev ◽  
Sivagowry Rasalingam Mørk ◽  
Kasper Pryds ◽  
Hussain Contractor ◽  
Jan Hansen ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Glyceryl Trinitrate ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Myocardium ◽  
Remote Ischemic Conditioning ◽  
Ischemic Conditioning ◽  
Human Endothelium

Remote ischemic conditioning (RIC) protects against sustained myocardial ischemia. Because of overlapping mechanisms, this protection may be altered by glyceryl trinitrate (GTN), which is commonly used in the treatment of patients with chronic ischemic heart disease. We investigated whether long-term GTN treatment modifies the protection by RIC in the rat myocardium and human endothelium. We studied infarct size (IS) in rat hearts subjected to global ischemia-reperfusion (I/R) in vitro and endothelial function in healthy volunteers subjected to I/R of the upper arm. In addition to allocated treatment, rats were coadministered with reactive oxygen species (ROS) or nitric oxide (NO) scavengers. Rats and humans were randomized to 1) control, 2) RIC, 3) GTN, and 4) GTN + RIC. In protocols 3 and 4, rats and humans underwent long-term GTN treatment for 7 consecutive days, applied subcutaneously or 2 h daily transdermally. In rats, RIC and long-term GTN treatment reduced mean IS (18 ± 12%, P = 0.007 and 15 ± 5%, P = 0.002) compared with control (35 ± 13%). RIC and long-term GTN treatment in combination did not reduce IS (29 ± 12%, P = 0.55 vs. control). ROS and NO scavengers both attenuated IS reduction by RIC and long-term GTN treatment. In humans, I/R reduced endothelial function ( P = 0.01 vs. baseline). Separately, RIC and long-term GTN prevented the reduction in endothelial function caused by I/R; given in combination, prevention was lost. RIC and long-term GTN treatment both protect against rat myocardial and human endothelial I/R injury through ROS and NO-dependent mechanisms. However, when given in combination, RIC and long-term GTN treatment fail to confer protection. NEW & NOTEWORTHY Remote ischemic conditioning (RIC) and long-term glyceryl trinitrate (GTN) treatment protect against ischemia-reperfusion injury in both human endothelium and rat myocardium. However, combined application of RIC and long-term GTN treatment abolishes the individual protective effects of RIC and GTN treatment on ischemia-reperfusion injury, suggesting an interaction of clinical importance.

Influence of phospholipase A2 and paraoxonase activity on endothelial function changes in various forms of coronary artery disease

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
VI Maslovskyi ◽  
IA Mezhiievska ◽  
YV Maslovskyi
Keyword(s):  
Coronary Artery Disease ◽  
Blood Flow ◽  
Coronary Artery ◽  
Endothelial Function ◽  
Phospholipase A2 ◽  
Brachial Artery ◽  
Vascular Disorders ◽  
Paraoxonase Activity ◽  
Artery Disease ◽  
Phospholipase A2 Activity

Abstract Funding Acknowledgements Type of funding sources: None. High phospholipase A2 activity is associated with atherosclerotic disorders of the arteries, while paraoxonase activity decreases with increasing atherogenic plasma activity. The purpose is to study the relationship between the combined effect of phospholipase A2 and paraoxonase activity on vascular endothelial dysfunction in various forms of coronary artery disease. We examined 152 men 52.5 ± 0.8 years, including 53 - STEMI, 32 - NSTEMI, 67 - chronic chronic coronary syndromes (CCS). Methods. All patients were examined for endothelial function of the brachial artery with a test for reactive hyperemia and vasodilation with exogenous NO, as well as determination of phospholipase A2 activity and plasma paraoxonase activity. All studiies conform to the principles of the Declaration of Helsinki of the World Medical Association. Results. Dynamics evaluation of endothelial function indicates a significant increase in blood flow in the brachial artery after compression in the NSTEMI group, but a decrease in the STEMI group after vasodilation of exogenous NO. Analysis of phospholipase A2 activity and paraoxonase showed an increasing the first in STEMI group compared to NSTEMI one and CCS while decreasing the second in the corresponding groups (Tab. 1). The results of the study confirm the association of increased activity of phospholipase A2 with vascular disorders severity, the correction of which should be considered a priority in prospective studies. The fact of reducing the activity of paraoxonase should be considered in the correction treatment of vascular disorders. Tab. 1 CCS NSTEMI STEMI LSD criteria D% 7,48 ± 0,39 6,65 ± 0,54 6,77 ± 0,62 {1-2} V% 54,71 ± 1,01 51,13 ± 1,92 42,16 ± 3,29 p1 &lt; 0,0001 p2 = 0,010 {3} / {1, 2} D% (NO) 10,35 ± 0,47 8,24 ± 0,96 10,28 ± 0,98 {1, 2} V% (NO) 55,60 ± 1,12 37,71 ± 3,72 p1 &lt; 0,0001 28,12 ± 3,94 p1 &lt; 0,0001 {1} / {2, 3} sPA2 1,12 ± 0,03 1,25 ± 0,04 p1 &lt; 0,0001 1,34 ± 0,04 p1 &lt; 0,0001 {1} / {2, 3} PAO 0,54 ± 0,01 0,50 ± 0,01 0,44 ± 0,01 p1 &lt; 0,0001 p2 &lt; 0,0001 {1} / {2,3} D% - diameter of brachial artery after compression. V% - blood flow velocity after compression. sPA2 -phospholipase A2. PAO - paraoxanase. p - reliability on Sheffe"s criteria.

Using the Talk Test to Prescribe and Guide Exercise Intensity: Speaking Your Way to Improved Fitness

2018 ◽  
Author(s):  
Nick Preobrazenski
Keyword(s):  
Exercise Intensity ◽  
Ventilatory Threshold ◽  
Peak Oxygen Consumption ◽  
Individual Level ◽  
Non Invasive ◽  
Before And After ◽  
Small Incidence ◽  
Three Stages ◽  
Physiological Markers ◽  
Healthy Males

Introduction: The Talk Test (TT) is a non-invasive, subjective method of prescribing exercise intensity. The TT involves three stages. When exercisers can speak comfortably, can speak but not comfortably, or cannot speak comfortably, they are in the positive (POS), equivocal (EQ), and negative (NEG) TT stages, respectively. The NEG stage correlates with important physiological markers such as ventilatory threshold and lactate threshold. Given the evidence demonstrating large increases peak oxygen consumption (VO2peak) when training at intensities above these markers, the purpose of the study was to test the hypothesis that the TT is efficacious for improving VO2peak at both the group and individual level in young, healthy males. Methods: 11 healthy males completed a maximal fitness test before and after 4 weeks of training 4 times per week for 30 minutes in the NEG stage. The TT was performed every 2.5 to 5 minutes to ensure that the resistance would be enough to elicit a NEG response. Changes in VO2peak below 2 times a previously established typical error were classified as non-response. Results: Four weeks of training at NEG induced a significant increase (11.5%) in VO2peak (PRE: 45.80 mL/Kg/min ± 4.92; POST 51.07 mL/Kg/min ± 5.45, p < 0.001). Furthermore, only one participant (9.09%) was classified as a non-responder in VO2peak following training. Conclusion: These results suggest that the TT can efficaciously prescribe and guide exercise intensity in young, healthy males, and that training at an intensity that prevents comfortable speech leads to a small incidence of non-response

Fenofibrate improves endothelial function in the brachial artery and forearm resistance arterioles of statin-treated Type 2 diabetic patients

2010 ◽  
Vol 118 (10) ◽  
pp. 607-615 ◽  
Author(s):  
Sandra J. Hamilton ◽  
Gerard T. Chew ◽  
Timothy M.E. Davis ◽  
Gerald F. Watts
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Statin Therapy ◽  
Brachial Artery ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

Dyslipidaemia contributes to endothelial dysfunction and CVD (cardiovascular disease) in Type 2 diabetes mellitus. While statin therapy reduces CVD in these patients, residual risk remains high. Fenofibrate corrects atherogenic dyslipidaemia, but it is unclear whether adding fenofibrate to statin therapy lowers CVD risk. We investigated whether fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. In a cross-over study, 15 statin-treated Type 2 diabetic patients, with LDL (low-density lipoprotein)-cholesterol <2.6 mmol/l and endothelial dysfunction [brachial artery FMD (flow-mediated dilatation) <6.0%] were randomized, double-blind, to fenofibrate 145 mg/day or matching placebo for 12 weeks, with 4 weeks washout between treatment periods. Brachial artery FMD and endothelium-independent NMD (nitrate-mediated dilatation) were measured by ultrasonography at the start and end of each treatment period. PIFBF (post-ischaemic forearm blood flow), a measure of microcirculatory endothelial function, and serum lipids, lipoproteins and apo (apolipoprotein) concentrations were also measured. Compared with placebo, fenofibrate increased FMD (mean absolute 2.1±0.6 compared with −0.3±0.6%, P=0.04), but did not alter NMD (P=0.75). Fenofibrate also increased maximal PIFBF {median 3.5 [IQR (interquartile range) 5.8] compared with 0.3 (2.1) ml/100 ml/min, P=0.001} and flow debt repayment [median 1.0 (IQR 3.5) compared with −1.5 (3.0) ml/100 ml, P=0.01]. Fenofibrate lowered serum cholesterol, triacylgycerols (triglycerides), LDL-cholesterol, apoB-100 and apoC-III (P≤0.03), but did not alter HDL (high-density lipoprotein)-cholesterol or apoA-I. Improvement in FMD was inversely associated with on-treatment LDL-cholesterol (r=−0.61, P=0.02) and apoB-100 (r=−0.54, P=0.04) concentrations. Fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. This may relate partly to enhanced reduction in LDL-cholesterol and apoB-100 concentrations.

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