scholarly journals Features of stress-regulating system changes in adolescents with cardiovascular pathology at endothelial dysfunction

2020 ◽  
pp. 8-14
Author(s):  
D. Kashkalda ◽  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Normal Function ◽  
The State ◽  
Vascular Pathology ◽  
Antioxidant Systems ◽  
Vascular Endothelial ◽  
System Changes ◽  
Endothelial Response

Relevance. Endothelial dysfunction serves as a starting mechanism for any vascular pathology and its progression. The state of endothelial function is greatly influenced by stress, however, the study of the features of the functioning of stress-regulating systems in adolescents with cardiovascular disorders has practically not been studied. Objective: to investigate stress-regulating system changes in adolescents with cardiovascular disease at endothelial dysfunction. Materials and methods. A total of 73 adolescents (49 boys and 24 girls) with cardiovascular disease (CVD) aged 12–18 were surveyed. The adolescents were divided into 3 groups: those with normal endothelial function, those with endothelial dysfunction and those with paradoxical vascular endothelial response. Stress regulation is dominated by stress- realizing and stress-limiting systems. The state of stress-realizing systems was assessed by the level of cortisol, malondialdehyde, carbonylated proteins (CP) in blood serum and catecholamines (CA) in urine; stress-limiting systems — by the level of glutathione peroxidase (GPO), superoxide dismutase (SOD), serotonin in the blood and melatonin in urine. Results. In adolescents with endothelial dysfunction and paradoxical vascular endothelial response, there was a regulatory imbalance of key antioxidant enzymes (SOD and GPO) and a decrease in serotonin levels. In endothelial vascular dysfunction, changes in stress-regulatory systems are more pronounced in girls. The revealed correlation relations of the studied indicators in adolescents with normal function and vascular endothelium dysfunction emphasize strong links between monoamines (CA and melatonin), enzymatic (GPO) tension and activation of non-enzymatic (melatonin) links of antioxidant system. Conclusion. In adolescents with a non-inflammatory pathology of CVD, endothelial function depends on the activation and interaction of stress-regulating systems. With vascular endothelial dysfunction, changes in the content of monoamines and indicators of the pro- and antioxidant systems have gender differences, indicating stress-limiting stress and activation of stress-realizing systems in girls. The research was carried out in accordance with the principles of the Helsinki Declaration. The study protocol was approved by the Local Ethics Committee of all participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the author. Key words: adolescents, cardiovascular system, endothelial function, stresslimiting indicators, stressrealizing indicators.

scholarly journals Endothelial dysfunction in patients with lymphoproliferative disorders and its changes in the course of polychemotherapy

2020 ◽  
Vol 9 (3) ◽  
Author(s):  
Igor L. Davydkin ◽  
Tatyana P. Kuzmina ◽  
Ksenia V. Naumova ◽  
Rais K. Khayretdinov ◽  
Olesya E. Danilova ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Lymphoproliferative Disorders ◽  
Vascular Endothelial ◽  
Cardiovascular Toxicity ◽  
Cardiovascular Damage ◽  
Before And After ◽  
Chemotherapeutic Treatment ◽  
Endothelial Growth Factor

The article is dedicated to contemporary views on the change of endothelial function in the patients with lymphoproliferative disorders prior to, and in the process of, chemotherapeutic treatment. Considering that possibilities of standard examination do not always help identifying subclinical endothelial dysfunction, it is necessary to use specific methods, in particular, to determine the levels of endothelin-1 and vascular endothelial growth factor to monitor endothelial function. The objective of this review is to identify problems and prospects for recognizing early subclinical changes of endothelial function in the patients with lymphoproliferative disorders before and after chemotherapy. Assessing presence and severity of endothelial dysfunction may be useful for determining subclinical stages of cardiovascular damage, stratifying the risk of the patients with confirmed cardiovascular disease, and reducing the likelihood of cardio- and endotheliotoxic effects in patients long after chemotherapy. That is why early detection and immediate therapy of cardiovascular toxicity is currently the most important task in the patients with lymphoproliferative disorders, receiving chemotherapy.

Sitagliptin improves vascular endothelial function in Japanese type 2 diabetes patients without cardiovascular disease

2012 ◽  
Vol 02 (03) ◽  
pp. 338-345 ◽  
Author(s):  
Kazunari Suzuki ◽  
Kentaro Watanabe ◽  
Tatsuya Suzuki ◽  
Motoshi Ouchi ◽  
Shoko Futami-Suda ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Endothelial Function ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Diabetes Patients

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives

2021 ◽  
Vol 320 (1) ◽  
pp. H29-H35
Author(s):  
Joshua M. Cherubini ◽  
Jem L. Cheng ◽  
Jennifer S. Williams ◽  
Maureen J. MacDonald
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Sleep Deprivation ◽  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Health Concern ◽  
Short Sleep ◽  
Inadequate Sleep

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/

scholarly journals Valvular endothelial cells and the mechanoregulation of valvular pathology

2007 ◽  
Vol 362 (1484) ◽  
pp. 1445-1457 ◽  
Author(s):  
Jonathan T Butcher ◽  
Robert M Nerem
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Endothelial Activation ◽  
Therapeutic Strategies ◽  
Vascular Pathology ◽  
Diagnostic Tools ◽  
Mechanical Stimuli ◽  
Endothelial Denudation ◽  
Endothelial Response ◽  
Valvular Diseases

Endothelial cells are critical mediators of haemodynamic forces and as such are important foci for initiation of vascular pathology. Valvular leaflets are also lined with endothelial cells, though a similar role in mechanosensing has not been demonstrated. Recent evidence has shown that valvular endothelial cells respond morphologically to shear stress, and several studies have implicated valvular endothelial dysfunction in the pathogenesis of disease. This review seeks to combine what is known about vascular and valvular haemodynamics, endothelial response to mechanical stimuli and the pathogenesis of valvular diseases to form a hypothesis as to how mechanical stimuli can initiate valvular endothelial dysfunction and disease progression. From this analysis, it appears that inflow surface-related bacterial/thrombotic vegetative endocarditis is a high shear-driven endothelial denudation phenomenon, while the outflow surface with its related calcific/atherosclerotic degeneration is a low/oscillatory shear-driven endothelial activation phenomenon. Further understanding of these mechanisms may help lead to earlier diagnostic tools and therapeutic strategies.

scholarly journals COVID-19 and its effects on endothelium in HIV-positive patients in sub-Saharan Africa: Cardiometabolic risk, thrombosis and vascular function (ENDOCOVID STUDY)

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Nandu Goswami ◽  
Per Morten Fredriksen ◽  
Knut E. A. Lundin ◽  
Chidozie Agu ◽  
Simiat Olanike Elias ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Endothelial Function ◽  
Hiv Infection ◽  
Sub Saharan Africa ◽  
System Capacity ◽  
People Living With Hiv ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Sub Saharan

Abstract Background COVID-19 has affected almost every country in the world, especially in terms of health system capacity and economic burden. People from sub-Saharan Africa (SSA) often face interaction between human immunodeficiency virus (HIV) infection and non-communicable diseases such as cardiovascular disease. Role of HIV infection and anti-retroviral treatment (ART) in altered cardiovascular risk is questionable and there is still need to further carry out research in this field. However, thus far it is unclear, what impact the COVID-19 co-infection in people living with HIV (PLHIV), with or without therapy will have. The ENDOCOVID project aims to investigate whether and how HIV-infection in COVID-19 patients modulates the time course of the disease, alters cardiovascular risk, and changes vascular endothelial function and coagulation parameters/ thrombosis risk. Methods A total of 1026 patients will be included into this study. Cardiovascular research PLHIV with (n = 114 in each of the three recruiting centers) - or without - ART (n = 114 in each of the three recruiting centers) with COVID-19 and HIV-negative with COVID-19 (n = 114 in each of the three recruiting centers) will be carried out via clinical and biochemical measurements for cardiovascular risk factors and biomarkers of cardiovascular disease (CVD). Vascular and endothelial function will be measured by brachial artery flow-mediated dilatation (FMD), carotid intima-media thickness (IMT) assessments, and retinal blood vessel analyses, along with vascular endothelial biomarkers and cogualation markers. The correlation between HIV-infection in COVID-19 PLHIV with or without ART and its role in enhancement of cardiovascular risk and endothelial dysfunction will be assessed at admission, weekly, at discharge and, 4 weeks post-discharge (if possible). Impact of project The ENDOCOVID project aims to evaluate in the long-term the cardiovascular risk and vascular endothelial function in PLHIV thus revealing an important transitional cardiovascular phenotype in COVID-19. The study was registered under clinicaltrials.gov (NCT04709302).

scholarly journals Endothelial function in normal and pathological conditions

2019 ◽  
pp. 154-159
Author(s):  
A. V. Pizov ◽  
N. A. Pizov ◽  
O. A. Skachkova ◽  
N. V. Pizovа
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Tone ◽  
Vascular Wall ◽  
The State ◽  
Vascular Growth ◽  
Pathological Conditions ◽  
Basic Functions

The article presents the data on the state of endothelial function in the normally and in various diseases and conditions. The basic  functions of endothelium in modulation of vascular tone, atrombogenicity and thrombogenicity of the vascular wall, regulation of  vascular wall adhesion, regulation of vascular growth are described. The main causes leading to the formation of endothelial  dysfunction and the mechanisms underlying it are highlighted. Numerous studies on the evaluation of endothelial function in  various diseases are presented. The basic methods of drug and non-drug correction of endothelial dysfunction are presented. 

scholarly journals Abstract 236: Aldehydes in Cigarette Smoke Impair Vascular Endothelial Function

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Poonam Rao ◽  
Pooneh Nabavizadeh Rafsanjani ◽  
Daniel Han ◽  
Suzaynn Schick ◽  
Matthew Springer
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Cigarette Smoke ◽  
Secondhand Smoke ◽  
Negative Control ◽  
Vascular Endothelial ◽  
Vascular Endothelial Function ◽  
Gas Generation ◽  
Post Exposure

Introduction: Exposure to tobacco and marijuana smoke impairs vascular endothelial function. While the particulate phase of smoke is heavily implicated, the role of volatile constituents is unclear. Smoke contains aldehydes, which are known to cause endothelial dysfunction. We explored whether two aldehydes found in smoke, acrolein and acetaldehyde, can induce endothelial dysfunction. Hypothesis: Aldehydes in smoke impair endothelial function. Methods: We exposed 4 groups of anesthetized rats to 3 ppm acrolein and 10-11.5 ppm acetaldehyde gases (concentrations relevant to levels in secondhand smoke), Marlboro Red cigarette sidestream smoke at modest levels (600 μg/m 3 PM2.5) as a positive control, and clean air through the gas generation system as a negative control. Exposure was continuous for 10 minutes. Endothelial function (flow-mediated dilation; FMD) was quantified pre- and post-exposure by measuring femoral artery diameter with ultrasound before and after 5 min of transient ischemia and expressed as % vasodilation. Results: Impairment of FMD was observed for acrolein (10.8±1.7(SD)% vs. 5.8±2.9%, p=.001), acetaldehyde (8.8±2.0% vs. 6.0±2.5%, p=.001), and cigarette smoke (9.4±2.9% vs. 5.8±2.0%, p=.002), but not for air (7.9±2.0% vs. 9±3.2%, p=.44) (figure; each colored line denotes a rat pre- and post-exposure; bars denote means). Conclusions: Acrolein and acetaldehyde at levels found in secondhand smoke impair endothelial function. Our results suggest that despite a potential role of particles, volatile aldehydes may mediate part of the endothelial dysfunction caused by exposure to smoke.

Vascular pathophysiology of hypertension

2017 ◽  
Author(s):  
Tomasz J. Guzik ◽  
Rhian M. Touyz
Keyword(s):  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Smooth Muscle ◽  
Inflammatory Responses ◽  
Clinical Symptoms ◽  
Peripheral Resistance ◽  
Vascular Stiffness ◽  
Vascular Pathology

Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.

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