scholarly journals The characteristic of endothelium-dependent vasodilatation in athletes and untrained volunteers

2018 ◽  
Vol 17 (4) ◽  
pp. 42-46
Author(s):  
V. V. Kologrivova ◽  
A. N. Zakharova ◽  
E. V. Pakhomova ◽  
V. N. Vasilyev ◽  
L. V. Kapilevich
Keyword(s):  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Physical Exercise ◽  
Strength Training ◽  
Vascular Endothelium ◽  
High Intensity ◽  
Adaptive Response ◽  
Track And Field ◽  
Vascular Disorders ◽  
Physical Exercises

It is shown that strength-training athletes and track and field athletes have endothelial dysfunction. The vascular endothelium activity is not related to the direction of physical exercises. At the same time, the dynamic physical exercise induces endothelium vasodilatation function in all groups. Apparently, it can be the adaptive response to regular high-intensity physical exercises. At the same time it is a risk factor for acute vascular disorders.

scholarly journals Chronic stress and endothelial dysfunction: mechanisms, experimental challenges, and the way ahead

2020 ◽  
Vol 319 (2) ◽  
pp. H488-H506
Author(s):  
Lucien Derek Sher ◽  
Hannah Geddie ◽  
Lukas Olivier ◽  
Megan Cairns ◽  
Nina Truter ◽  
...  
Keyword(s):  
Risk Factor ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Chronic Stress ◽  
Vascular Endothelium ◽  
Review Article ◽  
Preclinical Models ◽  
Primary Target ◽  
Response Systems ◽  
Underlying Mechanisms

Although chronic stress is an important risk factor for cardiovascular diseases (CVD) onset, the underlying mechanisms driving such pathophysiological complications remain relatively unknown. Here, dysregulation of innate stress response systems and the effects of downstream mediators are strongly implicated, with the vascular endothelium emerging as a primary target of excessive glucocorticoid and catecholamine action. Therefore, this review article explores the development of stress-related endothelial dysfunction by focusing on the following: 1) assessing the phenomenon of stress and complexities surrounding this notion, 2) discussing mechanistic links between chronic stress and endothelial dysfunction, and 3) evaluating the utility of various preclinical models currently employed to study mechanisms underlying the onset of stress-mediated complications such as endothelial dysfunction. The data reveal that preclinical models play an important role in our efforts to gain an increased understanding of mechanisms underlying stress-mediated endothelial dysfunction. It is our understanding that this provides a good foundation going forward, and we propose that further efforts should be made to 1) more clearly define the concept of stress and 2) standardize protocols of animal models with specific guidelines to better indicate the mental complications that are simulated.

scholarly journals EFFECT OF HIGH-INTENSITY EXERCISE ON ENDOTHELIAL FUNCTION IN PATIENTS WITH T2DM

2016 ◽  
Vol 22 (2) ◽  
pp. 126-130 ◽  
Author(s):  
Carlos Alberto da Silva ◽  
Francisco Sérgio Lopes Vasconcelos-Filho ◽  
Marcus Serafim ◽  
Edson Botura ◽  
Roberta Cristina da Rocha-e-Silva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Type 2 Diabetes Mellitus ◽  
Endothelial Dysfunction ◽  
Physical Exercise ◽  
Endothelial Function ◽  
High Intensity ◽  
Before And After

Introduction: Diabetes mellitus is the most common metabolic disease worldwide. Endothelial dysfunction characteristic of these patients is one of the major risk factors for atherosclerosis. Early diagnosis of endothelial dysfunction is essential for the treatment especially of non-invasive manner, such as flow mediated dilation. Physical exercise is capable of generating beneficial adaptations may improve endothelial function. Objective: Identify the effect of physical exercise, using the clinical technique of ultrasound in the assessment of the endothelial function of patients with metabolic syndrome or type 2 diabetes mellitus. Methods: Thirty-one patients with type 2 diabetes mellitus or metabolic syndrome were studied, with a mean age (± SD) of 58±6 years, randomized into three groups. The training was performed for 50 minutes, four times a week. Before and after six weeks of training, subjects performed the endurance test and a study of the endothelial function of the brachial artery by high-resolution ultrasound. Results: After hyperemia, the percentage of arterial diameter was significantly higher for the high-intensity group (HI before = 2.52±2.85mm and after = 31.81±12.21mm; LI before = 3.23±3.52mm and after = 20.61±7.76mm; controls before = 3.56±2.33mm and after = 2.43±2.14mm; p<0.05). Conclusions: The high-intensity aerobic training improved the vasodilatation response-dependent endothelium, recorded by ultrasound, in patients with metabolic syndrome and type 2 diabetes.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Labor intensity as a risk factor for the formation of cardiovascular disease of energy facility operators

2020 ◽  
pp. 662-662
Author(s):  
V. N. Krasnoshchekova ◽  
N. E. Ilyukhin
Keyword(s):  
Cardiovascular Disease ◽  
Risk Factor ◽  
Cardiovascular System ◽  
High Intensity ◽  
Power Plants ◽  
Labor Process ◽  
Labor Intensity ◽  
Operating Personnel ◽  
Emergency Situations ◽  
Energy Facility

The functional shifts of the cardiovascular system at high intensity of the labor process for the prevention of psycho-emotional stress of the operating personnel and the prevention of the danger of emergency situations at power plants were studied.

scholarly journals Sudden Cardiac Death Risk in Downhill Skiers and Mountain Hikers and Specific Prevention Strategies

2021 ◽  
Vol 18 (4) ◽  
pp. 1621
Author(s):  
Josef Niebauer ◽  
Martin Burtscher
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Sudden Cardiac Death ◽  
High Intensity ◽  
Cardiac Death ◽  
High Intensity Exercise ◽  
Systemic Hypertension ◽  
Physical Strain ◽  
Mountainous Regions ◽  
Downhill Skiing

Sudden cardiac death (SCD) still represents an unanticipated and catastrophic event eliciting from cardiac causes. SCD is the leading cause of non-traumatic deaths during downhill skiing and mountain hiking, related to the fact that these sports are very popular among elderly people. Annually, more than 40 million downhill skiers and mountain hikers/climbers visit mountainous regions of the Alps, including an increasing number of individuals with pre-existing chronic diseases. Data sets from two previously published case-control studies have been used to draw comparisons between the SCD risk of skiers and hikers. Data of interest included demographic variables, cardiovascular risk factors, medical history, physical activity, and additional symptoms and circumstances of sudden death for cases. To establish a potential connection between the SCD risk and sport-specific physical strain, data on cardiorespiratory responses to downhill skiing and mountain hiking, assessed in middle-aged men and women, have been included. It was demonstrated that previous myocardial infarction (MI) (odds ratio; 95% CI: 92.8; 22.8–379.1; p < 0.001) and systemic hypertension (9.0; 4.0–20.6; p < 0.001) were predominant risk factors for SCD in skiers, but previous MI (10.9; 3.8–30.9; p < 0.001) and metabolic disorders like hypercholesterolemia (3.4; 2.2–5.2; p < 0.001) and diabetes (7.4; 1.6–34.3; p < 0.001) in hikers. More weekly high-intensity exercise was protective in skiers (0.17; 0.04–0.74; p = 0.02), while larger amounts of mountain sports activities per year were protective in hikers (0.23; 0.1–0.4; <0.001). In conclusion, previous MI history represents the most important risk factor for SCD in recreational skiers and hikers as well, and adaptation to high-intensity exercise is especially important to prevent SCD in skiers. Moreover, the presented differences in risk factor patterns for SCDs and discussed requirements for physical fitness in skiers and hikers will help physicians to provide specifically targeted advice.

Mercury Exposure and Endothelial Dysfunction

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Vascular Endothelium ◽  
Circulatory System ◽  
Vital Role ◽  
Mercury Exposure ◽  
And Function ◽  
The Impact ◽  
And Oxidative Stress

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.

scholarly journals Differential involvement of COX1 and COX2 in the vasculopathy associated with the α-galactosidase A-knockout mouse

2009 ◽  
Vol 296 (4) ◽  
pp. H1133-H1140 ◽  
Author(s):  
James L. Park ◽  
Liming Shu ◽  
James A. Shayman
Keyword(s):  
Endothelial Dysfunction ◽  
Fabry Disease ◽  
Vascular Endothelium ◽  
Vascular Function ◽  
Knockout Mouse ◽  
Vascular Reactivity ◽  
Lysosomal Storage ◽  
Wild Type ◽  
Cox Inhibitors ◽  
Differential Involvement

The lysosomal storage disorder Fabry disease is characterized by excessive globotriaosylceramide (Gb3) accumulation in major organs such as the heart and kidney. Defective lysosomal α-galactosidase A (Gla) is responsible for excessive Gb3 accumulation, and one cell sensitive to the effects of Gb3 accumulation is vascular endothelium. Endothelial dysfunction is associated with Fabry disease and excessive cellular Gb3. We previously demonstrated that excessive vascular Gb3 in a mouse model of Fabry disease, the Gla-knockout ( Gla−/0) mouse, results in abnormal vascular function, which includes abnormal endothelium-dependent contractions, a vascular phenomenon known to involve cyclooxygenase (COX). Therefore, we hypothesized that the vasculopathy in the Gla knockout mouse may be due to a vasoactive COX-derived product. To test this hypothesis, vascular reactivity experiments were performed in aortic rings from wild-type ( Gla+/0) and Gla−/0 mice in the presence and absence of specific and nonspecific COX inhibitors. Specific inhibition of COX1 or COX2 in endothelium-intact rings from Gla−/0 mice decreased overall phenylephrine contractility compared with untreated Gla−/0 rings, whereas COX inhibitors had no effect on contractility in endothelium-denuded rings. Nonspecific inhibition of COX with indomethacin (10 μmol/l) or COX1 inhibition with valeryl salicylate (3 mmol/l) improved endothelial function in rings from Gla−/0 mice, but COX2 inhibition with NS-398 (1 μmol/l) further increased endothelial dysfunction in rings from Gla−/0 mice. These results suggest that, in the Gla−/0 mice, COX1 and COX2 activity are increased and localized in the endothelium, producing vasopressor and vasorelaxant products, which contribute to the Fabry-related vasculopathy.

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