scholarly journals Morning impairment in vascular function is unrelated to overnight sleep or the inactivity that accompanies sleep

2018 ◽  
Vol 315 (5) ◽  
pp. R986-R993 ◽  
Author(s):  
Saurabh S. Thosar ◽  
Alec M. Berman ◽  
Maya X. Herzig ◽  
Sally A. Roberts ◽  
Michael R. Lasarev ◽  
...  

Adverse cardiovascular events, such as myocardial infarction and sudden cardiac death, occur more frequently in the morning. Prior studies have shown that vascular endothelial function (VEF), a marker of cardiovascular disease, is attenuated during physical inactivity and declines across the night. We sought to determine whether a morning attenuation in VEF is a result of prior sleep or the inactivity that inevitably accompanies sleep. After 1 wk of a rigorously controlled sleep-wake schedule and behaviors, 10 healthy participants completed a randomized crossover protocol in dim light and constant conditions, incorporating a night of 6 h of sleep opportunity and a night of immobility while they were supine and awake. VEF was measured in the dominant brachial artery as flow mediated dilation (FMD) before and after each 6-h trial. To avoid disturbing sleep and posture of the participants, blood was drawn using a 12-ft catheter from an adjoining laboratory room before, during, and after each 6-h trial, and plasma was analyzed for markers of oxidative stress [malondialdehyde adducts (MDA)], and endothelin-1. Contrary to expectation, both nocturnal sleep and nocturnal inactivity significantly increased FMD ( P < 0.05). There was no significant change in MDA or endothelin-1 within and between trials. Contrary to expectations based on prior studies, we found that overnight sleep or the inactivity that accompanies sleep did not result in attenuation in VEF in the morning hours in healthy people. Thus, it is plausible that the endogenous circadian system, a remaining factor not studied here, is responsible for the commonly observed decline in VEF across the night.

2017 ◽  
Vol 122 (2) ◽  
pp. 354-360 ◽  
Author(s):  
Steven K. Nishiyama ◽  
Jia Zhao ◽  
D. Walter Wray ◽  
Russell S. Richardson

Endothelin-1 (ET-1), a potent vasoconstrictor secreted by vascular endothelial cells, has been implicated in the pathophysiology of numerous cardiovascular diseases, yet the direct impact of ET-1 on vascular function remains unclear. Therefore, in seven young (23 ± 1 yr) healthy subjects, we investigated the effect of an intra-arterial infusion of ET-1 on reactive hyperemia (RH) and flow-mediated dilation (FMD) in the popliteal artery following 5 min of suprasystolic cuff occlusion. ET-1 infusion significantly attenuated basal leg blood flow (control: 62 ± 4 ml/min, ET-1: 47 ± 9 ml/min), RH [area-under-curve (AUC); control: 162 ± 15 ml, ET-1: 104 ± 16 ml], and peak RH (control: 572 ± 51 ml/min, ET-1: 412 ± 32 ml/min) ( P < 0.05). Administration of ET-1 also reduced FMD (control: 2.4 ± 0.3%, ET-1: 0.5 ± 0.5%) and FMD normalized for shear rate (control: 10.5 × 10−4 ± 2.0 × 10−4%/s−1, ET-1: 0.9 × 10−4 ± 2.8 ×10−4%/s−1). These findings reveal that elevated levels of ET-1 have a significant impact on vascular function, indicating that studies employing RH and FMD as markers of microvascular function and nitric oxide bioavailability, respectively, should exercise caution, as ET-1 can impact these assessments by tipping the balance between vasodilation and vasoconstriction, in favor of the latter. NEW & NOTEWORTHY Endothelin-1 (ET-1) is recognized as the body’s most potent endogenous vasoconstrictor, but the impact of this peptide on vascular function is not well understood. The present study revealed that the intra-arterial administration of ET-1 impaired both microvascular and conduit vessel function of the leg in young, healthy, humans. Studies employing vascular testing in patient cohorts that experience a disease-related increase in ET-1 should thus exercise caution, as ET-1 clearly impairs vascular function.


2007 ◽  
Vol 103 (5) ◽  
pp. 1655-1661 ◽  
Author(s):  
Takanobu Okamoto ◽  
Mitsuhiko Masuhara ◽  
Komei Ikuta

Aerobic exercise training combined with resistance training (RT) might prevent the deterioration of vascular function. However, how aerobic exercise performed before or after a bout of RT affects vascular function is unknown. The present study investigates the effect of aerobic exercise before and after RT on vascular function. Thirty-three young, healthy subjects were randomly assigned to groups that ran before RT (BRT: 4 male, 7 female), ran after RT (ART: 4 male, 7 female), or remained sedentary (SED: 3 male, 8 female). The BRT and ART groups performed RT at 80% of one repetition maximum and ran at 60% of the targeted heart rate twice each week for 8 wk. Both brachial-ankle pulse wave velocity (baPWV) and flow-mediated dilation (FMD) after combined training in the BRT group did not change from baseline. In contrast, baPWV after combined training in the ART group reduced from baseline (from 1,025 ± 43 to 910 ± 33 cm/s, P < 0.01). Moreover, brachial artery FMD after combined training in the ART group increased from baseline (from 7.3 ± 0.8 to 9.6 ± 0.8%, P < 0.01). Brachial artery diameter, mean blood velocity, and blood flow in the BRT and ART groups after combined training increased from baseline ( P < 0.05, P < 0.01, and P < 0.001, respectively). These values returned to the baseline during the detraining period. These values did not change in the SED group. These results suggest that although vascular function is not improved by aerobic exercise before RT, performing aerobic exercise thereafter can prevent the deteriorating of vascular function.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8725
Author(s):  
Therese Ruane-O’Hora ◽  
Ahmad Ahmeda ◽  
Farouk Markos

Background The role of the glycocalyx as the endothelial sensor of an increase in blood flow was assessed in the iliac artery in vivo. Methods Acetylcholine-induced flow mediated dilation was evaluated before and after vascular glycocalyx disruption. This was accomplished by exposing the iliac lumen to the chemotactic agent fMLP (1 μM; n = 6 pigs), concomitant heparinase III (100 mU ml−1) and hyaluronidase (14 mg ml−1) (n = 4), and neuraminidase (140 mU ml−1; n = 5), for 20 min in separate iliac artery preparations. Only one lumen intervention per iliac was conducted. Results For the heparinase III + hyaluronidase experiment, the iliac diameter increased by an average of 0.54 ± 0.11 mm before and 0.45 ± 0.03 mm after the enzymes (P = 0.42; paired Student’s t test). The iliac diameter increased by 0.31 ± 0.02 mm before and 0.29 ± 0.07 mm after fMLP exposure (P = 0.7) and the diameter increased by 0.54 ± 0.11 mm before and 0.54 ± 0.09 mm after neuraminidase exposure (P = 0.98). In all cases, the shear stress changes before and after lumen exposure were not significantly different to each other. Conclusion There was no significant reduction in flow mediated dilation of the iliac in response to any of the interventions conducted. Therefore, the vascular endothelial glycocalyx as whole is not required for flow mediated dilation in conduit arteries in the intact animal.


Author(s):  
Alexandra M. Coates ◽  
Heather L. Petrick ◽  
Philip J. Millar ◽  
Jamie F. Burr

Acute elevations in inflammatory cytokines have been demonstrated to increase aortic and left ventricular stiffness and reduce endothelial function in healthy subjects. As vascular and cardiac function are often transiently reduced following prolonged exercise, it is possible that cytokines released during exercise may contribute to these alterations. The a priori aims of this study were to determine if vaccine-induced increases in inflammatory-cytokines would reduce vascular and left ventricular function, whether vascular alterations would drive cardiac impairments, and whether this would be potentiated by moderate exercise. In a randomized cross-over fashion, sixteen male participants were tested under control (CON) and inflammatory (INF) conditions, wherein INF testing occurred 8h following administration of an influenza vaccine. On both days, participants underwent measures of echocardiography performed during light cycling (stress-echocardiography), carotid-femoral pulse wave velocity (cf-PWV), and superficial femoral flow-mediated dilation (FMD) before and after cycling for 90min at ~85% of their first ventilatory threshold. IL-6 increased significantly (∆1.9±1.3pg/mL, P<0.001), while TNFα was non-significantly augmented (∆0.05±0.11pg/mL, P=0.09), 8h following vaccination. Vascular function was unaltered following cycling or inflammation (all P>0.05). The use of echocardiography during light cycling revealed cardiac alterations traditionally expected to occur only with greater exercise loads, with reduced systolic (e.g. longitudinal strain CON:∆3.3±4.4%, INF:∆1.7±2.7%, P=0.002) and diastolic function (e.g. E/A ratio CON:∆-0.32±0.34a.u., INF:∆-0.25±0.27a.u., P=0.002) following cycling, independent of inflammation. The vaccine reduced stroke volume (SV) (main effect of condition P=0.009) before-and-after cycling. These findings indicate that reduced cardiac function following exercise occurs largely independent of additional inflammatory load.


Author(s):  
Tadakatsu Inagaki ◽  
James T. Pearson ◽  
Hirotsugu Tsuchimochi ◽  
Daryl O. Schwenke ◽  
Shigeyoshi Saito ◽  
...  

BACKGROUND: Pulmonary hypertension (PH) causes cardiac hypertrophy in the right ventricle (RV), and eventually leads to RV failure due to persistently elevated ventricular afterload. We hypothesized that the mechanical stress on the RV associated with increased afterload impairs vasodilator function of the right coronary artery (RCA) in PH. METHODS AND RESULTS: Coronary vascular response was assessed using microangiography with synchrotron radiation in two well-established PH rat models, monocrotaline injection or the combined exposure to chronic hypoxia and vascular endothelial growth factor receptor blockade with Su5416 (SuHx model). In the SuHx model, the effect of the treatment with the non-selective endothelin-1 receptor antagonist (ERA), macitentan was also examined. Myocardial viability was determined in SuHx model rats, using 18F-FDG PET and MRI. Endothelium-dependent and -independent vasodilator responses were significantly attenuated in the medium and small arteries of severe PH rats. ERA treatment significantly improved RCA vascular function compared to the untreated group. ERA treatment improved both the decrease in ejection fraction and the increased glucose uptake, and reduced RV remodeling. In addition, the upregulation of inflammatory genes in the RV was almost suppressed by ERA treatment. CONCLUSION: We found impairment of vasodilator responses in the RCA of severe PH rat models. Endothelin-1 activation in the RCA plays a major role in impaired vascular function in PH rats and is partially restored by ERA treatment. Treatment of PH with ERA may improve RV function in part by indirectly attenuating right heart afterload and in part by associated improvements in right coronary endothelial function.


2021 ◽  
Author(s):  
Isabel Witvrouwen ◽  
Dominique Mannaerts ◽  
Jessica Ratajczak ◽  
Evi Boeren ◽  
Ellen Faes ◽  
...  

In preeclampsia (PE) pre-existent maternal endothelial dysfunction leads to impaired placentation and vascular maladaptation. The vascular endothelial growth factor (VEGF) pathway is essential in the placentation process and VEGF expression is regulated through post-transcriptional modification by microRNAs. We investigated the expression of VEGF related circulating miR-16, miR-29b, miR-126, miR-155 and miR-200c in PE versus healthy pregnancies (HP), and their relation with vascular function, oxidative stress and systemic inflammation.In this case-control study, 24 women with early PE (in vivo vascular function (flow mediated dilation (FMD), modified FMD (mFMD), carotid-femoral pulse wave velocity (CF-PWV), augmentation index (AIx75) and reactive hyperaemia index (RHI)). FMD, CF-PWV, AIx75 and RHI were all significantly impaired in PE (p&lt;0.05). PE patients had reduced levels of miR-16 (5.53±0.36vs5.84±0.61) and increased levels of miR-200c (1.34±0.57vs0.97±0.68) (p&lt;0.05). Independent of age and parity, miR-16 was related to impaired FMD (ß 2.771, 95% C.I. 0.023-5.519, p=0.048) and mFMD (ß3.401, 95% C.I. 0.201-6.602, p=0.038). Likewise, miR-200c was independently associated with CF-PWV (ß0.513, 95% C.I. 0.034-0.992, p=0.036). In conclusion, circulating levels of miR-16 were lower in PE, which correlated with impaired endothelial function. Circulating miR-200c was increased in PE and correlated with higher arterial stiffness. These findings suggest a post-transcriptional dysregulation of the VEGF pathway in PE and identify miR-16 and miR-200c as possible diagnostic biomarkers for PE.


Author(s):  
Kyounghwa Jung ◽  
Jisu Kim ◽  
Hun-Young Park ◽  
Won-Sang Jung ◽  
Kiwon Lim

This study examined the effect of Pilates training under hypoxia, a novel treatment method, for obesity. Thirty-two Korean women with obesity (age: 34–60 (47.5 ± 7.5) years) were randomly assigned to control (CON; n = 10), normoxic Pilates training (NPTG; n = 10), and hypoxic Pilates training groups (HPTG; n = 12). The NPTG and HPTG performed 50 min of Pilates training using a tubing band for 12 weeks (3 days/week) in their respective environmental conditions (NPTG: normoxic condition, inspired oxygen fraction (FiO2) = 20.9%; HPTG: moderate hypoxic condition, FiO2 = 14.5%). The CON maintained their daily lifestyle without intervention. All subjects underwent body composition, blood pressure, arterial stiffness, vascular endothelial function, cardiometabolic biomarker, hemorheological function, and aerobic performance measurements before and after the intervention. The HPTG showed a significant improvement in diastolic blood pressure, total cholesterol and triglyceride concentrations, flow-mediated dilation, and erythrocyte deformability and aggregation (all p < 0.05) compared with the CON and NPTG. However, compared with the CON and NPTG, the HPTG did not show improvement in other parameters. Hypoxic Pilates intervention is a novel and successful method for promoting endothelial and hemorheological functions in women with obesity.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1872 ◽  
Author(s):  
Maho Sasaki ◽  
Yuri Nonoshita ◽  
Takashi Kajiya ◽  
Nobuhiko Atsuchi ◽  
Megumi Kido ◽  
...  

Vascular disease poses a major public health problem worldwide. Trigonelline isolated from Raphanus sativus cv. Sakurajima Daikon (Sakurajima radish) induces nitric oxide production from vascular endothelial cells and enhances vascular function. Here, we investigated the characteristics of trigonelline and its effects on endothelial function after consumption of Sakurajima radish by humans. Our results show that Sakurajima radish contains approximately 60 times more trigonelline than other radishes and squashes. Additionally, no significant differences were observed between varieties of Sakurajima radish, suggesting that any type of Sakurajima radish can be ingested for trigonelline supplementation. The effects of cooking and processing Sakurajima radish were also evaluated, as were the effects of freezing, and changes in osmotic pressure and pH. A first-in-human trial using Sakurajima radish showed that ingestion of 170 g/day of Sakurajima radish for ten days increased blood trigonelline concentrations and significantly improved flow-mediated dilation, which is a measure of vascular endothelial function. Overall, our findings suggest that the trigonelline contained in Sakurajima radish may contribute to improved human vascular endothelial function. Hence, Sakurajima radish may enhance vascular endothelial function as a functional food.


2019 ◽  
Vol 41 (26) ◽  
pp. 2472-2483 ◽  
Author(s):  
Marin Kuntic ◽  
Matthias Oelze ◽  
Sebastian Steven ◽  
Swenja Kröller-Schön ◽  
Paul Stamm ◽  
...  

Abstract Aims Electronic (e)-cigarettes have been marketed as a ‘healthy’ alternative to traditional combustible cigarettes and as an effective method of smoking cessation. There are, however, a paucity of data to support these claims. In fact, e-cigarettes are implicated in endothelial dysfunction and oxidative stress in the vasculature and the lungs. The mechanisms underlying these side effects remain unclear. Here, we investigated the effects of e-cigarette vapour on vascular function in smokers and experimental animals to determine the underlying mechanisms. Methods and results Acute e-cigarette smoking produced a marked impairment of endothelial function in chronic smokers determined by flow-mediated dilation. In mice, e-cigarette vapour without nicotine had more detrimental effects on endothelial function, markers of oxidative stress, inflammation, and lipid peroxidation than vapour containing nicotine. These effects of e-cigarette vapour were largely absent in mice lacking phagocytic NADPH oxidase (NOX-2) or upon treatment with the endothelin receptor blocker macitentan or the FOXO3 activator bepridil. We also established that the e-cigarette product acrolein, a reactive aldehyde, recapitulated many of the NOX-2-dependent effects of e-cigarette vapour using in vitro blood vessel incubation. Conclusions E-cigarette vapour exposure increases vascular, cerebral, and pulmonary oxidative stress via a NOX-2-dependent mechanism. Our study identifies the toxic aldehyde acrolein as a key mediator of the observed adverse vascular consequences. Thus, e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. Since e-cigarette use is increasing, particularly amongst youth, our data suggest that aggressive steps are warranted to limit their health risks.


2017 ◽  
Vol 312 (5) ◽  
pp. R828-R834 ◽  
Author(s):  
Martijn F. H. Maessen ◽  
Anke C. C. M. van Mil ◽  
Yaïra Straathof ◽  
Niels P. Riksen ◽  
Gerard A. P. J. M. Rongen ◽  
...  

Reperfusion is essential for ischemic tissue survival, but causes additional damage to the endothelium [i.e., ischemia-reperfusion (I/R) injury]. Ischemic preconditioning (IPC) refers to short repetitive episodes of ischemia that can protect against I/R. However, IPC efficacy attenuates with older age. Whether physical inactivity contributes to the attenuated efficacy of IPC to protect against I/R injury in older humans is unclear. We tested the hypotheses that lifelong exercise training relates to 1) attenuated endothelial I/R and 2) maintained IPC efficacy that protects veteran athletes against endothelial I/R. In 18 sedentary male individuals (SED, <1 exercise h/wk for >20 yr, 63 ± 7 yr) and 20 veteran male athletes (ATH, >5 exercise h/wk for >20 yr, 63 ± 6 yr), we measured brachial artery endothelial function with flow-mediated dilation (FMD) before and after I/R. We induced I/R by 20 min of ischemia followed by 20 min of reperfusion. Randomized over 2 days, participants underwent either 35-min rest or IPC (3 cycles of 5-min cuff inflation to 220 mmHg with 5 min of rest) before I/R. In SED, FMD decreased after I/R [median (interquartile range)]: [3.0% (2.0–4.7) to 2.1% (1.5–3.9), P = 0.046] and IPC did not prevent this decline [4.1% (2.6–5.2) to 2.8% (2.2–3.6), P = 0.012]. In ATH, FMD was preserved after I/R [3.0% (1.7–5.4) to 3.0% (1.9–4.1), P = 0.82] and when IPC preceded I/R [3.2% (1.9–4.2) to 2.8% (1.4–4.6), P = 0.18]. These findings indicate that lifelong exercise training is associated with increased tolerance against endothelial I/R. These protective, preconditioning effects of lifelong exercise against endothelial I/R may contribute to the cardioprotective effects of exercise training.


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