scholarly journals The state of cytokine regulation and endothelial dysfunction in the combined course of vibration disease and arterial hypertension

2021 ◽  
Vol 93 (6) ◽  
pp. 693-698
Author(s):  
Sergei A. Babanov ◽  
Rimma A. Baraeva ◽  
Leonid A. Strizhakov ◽  
Sergei V. Moiseev ◽  
Viktor V. Fomin
Keyword(s):  
Endothelial Dysfunction ◽  
Early Diagnosis ◽  
Arterial Hypertension ◽  
Inflammatory Cytokines ◽  
Endothelial Damage ◽  
The State ◽  
Cytokine Regulation ◽  
Vibration Disease ◽  
Willebrand Factor ◽  
Cytokine Imbalance

Background. The article presents data on the state of cytokine regulation, indicators of endothelial damage when exposed to industrial vibration (general, local) and in combination with arterial hypertension. Aim. To improve the quality of early diagnosis and prevention of vibration disease in an isolated course and its combination with arterial hypertension based on a study of the cytokine profile, biomarkers of endothelial dysfunction in this pathology. Materials and methods. A comprehensive survey of 84 patients with isolated vibration disease from the effects of local, general, first, second degree and 61 patients with a combined course of vibration disease from the effects of local, general second degree vibration and arterial hypertension, 30 people in the control group without contact with industrial vibration and found healthy by medical examination. The levels of pro-inflammatory (IL-1, IL-8, TNF-) and anti-inflammatory cytokines (IL-4), biomarkers of endothelial damage (EDN-1, TGF-1, VEGF-A, PDGF-BB, fibronectin, Willebrand factor) were determined using the enzyme immunoassay method. Results. The response of the immune system to the effects of industrial vibration is characterized by a cytokine imbalance an increase in the level of pro-inflammatory cytokines (IL-1, IL-8, TNF-) and a decrease in the level of anti-inflammatory cytokine (IL-4). With a combined course of vibratory disease and arterial hypertension, the cytokine imbalance is characterized by an even more significant increase in serum IL-1, IL-8, TNF- and a decrease in serum IL-4 concentration. Endothelial dysfunction with WB from the action of both local and general vibration in combination with hypertension is characterized by a significant increase in serum EDN-1, TGF-1, VEGF-A, PDGF-BB, fibronectin, Willebrand factor. Conclusion. The study of the cytokine profile, biomarkers of damage to the vascular endothelium in this pathology will allow for the early diagnosis of vascular disorders and to optimize preventive measures for workers in vibration-hazardous industries.

scholarly journals Correction of endothelial function in hypertension associated with tyberculosis by fixed combination of perindopril and indopamide

2007 ◽  
Vol 13 (4) ◽  
pp. 256-261
Author(s):  
N. YU. Klimenko ◽  
N. V. Drobotya ◽  
A. A. Kastanyan ◽  
V. V. Kaltykova ◽  
E. Sh. Guseynova
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Arterial Hypertension ◽  
Von Willebrand Factor ◽  
Fixed Combination ◽  
Factor Level ◽  
Hypertensive Patients ◽  
Von Willebrand ◽  
Willebrand Factor

A study of daily blood pressure (BP) dynamics, functional endothelial condition at hypertensive patients in combination with tuberculosis of various localization and estimation of an opportunity of correction of the revealed disturbances during 12-week therapy by the fixed combination of perindopril and indapamide - noliprel-forte (Servier, France) were performed. During research more expressed endothelial dysfunction at hypertensive patients, proceeding on a background of tubercular process in comparison with patients with isolated arterial hypertension was revealed. Therapy by noliprel-forte provided the reliable 24-hour control of BP level, which was accompanied by endothelial function normalization that was shown by improvement of a endothelium-dependent vasodilatation and decrease of a von Willebrand factor level. .

Evidence of Endothelial Dysfunction in Cocaine Users.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1891-1891 ◽  
Author(s):  
Jai me Pereira ◽  
Claudia G. Sáez ◽  
Julio Pallavicini ◽  
Paulina Olivares ◽  
Olga Panes ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Von Willebrand Factor ◽  
Peripheral Blood ◽  
Endothelial Damage ◽  
Cocaine Users ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Plasma Markers

Abstract Background: Cocaine abuse is associated with an increased risk of cardiac and cerebrovascular events, such as myocardial infarction, sudden cardiac death, and ischemic stroke. The underlying mechanisms leading to these complications are not fully understood although intravascular thrombus formation and accelerated atherosclerosis are prominent findings. In this sense, in vitro studies have demonstrated that cocaine may induce damage and/or activation of endothelial cells. The structural and functional integrity of the endothelium is essential for the maintenance of vascular homeostasis and its damage plays a critical role in the pathogenesis of vascular disease. Endothelial dysfunction may be assessed by testing the impaired vasodilator response to a stimulus or by measuring the release of plasma markers of endothelial damage. Increased number of circulating endothelial cells (CECs) has been reported in several pathologic conditions associated with severe vascular damage and its enumeration in peripheral blood is currently considered a reliable method to assess endothelial damage. We hypothesized that chronic exposure to cocaine induces endothelial damage which could be expressed by increased CEC counts in peripheral blood. Methods: Twenty cocaine-dependent subjects (aged 19–52 years, mean age 30 years) and 25 healthy, matched controls (aged 20–49 years, mean age 31 years) were studied; all patients fulfilled DSM-IV criteria for cocaine dependence with drug exposure within the 72 hours prior to blood sampling. CECs were isolated from peripheral blood by use of immunomagnetic beads coated with anti-CD146, stained for CD45 and Ulex Europaeus lectin 1 and counted under fluorescence microscopy. MCP-1, sICAM-1, von Willebrand factor and high-sensitivity C-reactive protein (hsCRP) were measured by enzyme-linked immunosorbent assay. Results: Compared to controls, CECs were significantly elevated among cocaine users (632 ± 281 vs 67 ± 54 cells/mL, p<0.0001). Plasma levels of sICAM-1 (360±92 ng/mL) and MCP-1 (166±71 pg/mL) were increased in cocaine-dependent individuals compared to the controls (261±34 and 67±29, respectively; p< 0.01). The hsCRP levels were significantly increased (6.8 mg/L); however plasma von Willebrand factor concentration was not different between patients and controls (86.4±22 vs 70.5±16%, respectively; NS). Levels of CECs correlated positively with sICAM-1 (r: 0.7; p: 0.003) and hsCRP (r: 0.56; p: 0.0037). Conclusions: Highly increased number of CECs and significant increments in soluble plasma markers of endothelial perturbation were found in cocaine dependent individuals. This is the first demonstration of endothelial dysfunction among these individuals and our findings support the notion that cocaine-induced endothelial damage may play a pathogenic role in the ischemic vascular disease observed in chronic cocaine users.

The changes of some indicators of endothelial dysfunction in response to physical activity in individuals with arterial hypertension

2019 ◽  
Vol 25 (1) ◽  
pp. 17-22
Author(s):  
I.S. Dronyk ◽  
◽  
O.Y. Yavorsky ◽  
O.Y. Sklyarov ◽  
R.S. Pshyk ◽  
...  
Keyword(s):  
Physical Activity ◽  
Endothelial Dysfunction ◽  
Arterial Hypertension

Endothelial Dysfunction and Inflammatory Markers of Vascular Disease

2020 ◽  
Vol 19 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Sevket Balta
Keyword(s):  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Inflammatory Markers ◽  
Vascular Diseases ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Non Invasive ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor

: Vascular diseases are the main reason for morbidity and mortality worldwide. As we know, the earlier phase of vascular diseases is endothelial dysfunction in humans, the endothelial tissues play an important role in inflammation, coagulation, and angiogenesis, via organizing ligand-receptor associations and the various mediators’ secretion. We can use many inflammatory non-invasive tests (flowmediated dilatation, epicedial fat thickness, carotid-intima media thickness, arterial stiffness and anklebrachial index) for assessing the endothelial function. In addition, many biomarkers (ischemia modified albumin, pentraxin-3, E-selectin, angiopoietin, endothelial cell specific molecule 1, asymmetrical dimethylarginine, von Willebrand factor, endothelial microparticles and endothelial progenitor cells) can be used to evaluate endothelial dysfunction. We have focused on the relationship between endothelial dysfunction and inflammatory markers of vascular disease in this review.

scholarly journals Endothelial Dysfunction, Atherosclerosis, and Increase of von Willebrand Factor and Factor VIII: A Randomized Controlled Trial in Swine

2021 ◽  
Author(s):  
Ferdows Atiq ◽  
Jens van de Wouw ◽  
Oana Sorop ◽  
Ilkka Heinonen ◽  
Moniek P. M. de Maat ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Randomized Controlled Trial ◽  
Endothelial Dysfunction ◽  
Controlled Trial ◽  
Short Term ◽  
Randomized Controlled ◽  
Von Willebrand ◽  
Willebrand Factor

AbstractIt is well known that high von Willebrand factor (VWF) and factor VIII (FVIII) levels are associated with an increased risk of cardiovascular disease. It is still debated whether VWF and FVIII are biomarkers of endothelial dysfunction and atherosclerosis or whether they have a direct causative role. Therefore, we aimed to unravel the pathophysiological pathways of increased VWF and FVIII levels associated with cardiovascular risk factors. First, we performed a randomized controlled trial in 34 Göttingen miniswine. Diabetes mellitus (DM) was induced with streptozotocin and hypercholesterolemia (HC) via a high-fat diet in 18 swine (DM + HC), while 16 healthy swine served as controls. After 5 months of follow-up, FVIII activity (FVIII:C) was significantly higher in DM + HC swine (5.85 IU/mL [5.00–6.81]) compared with controls (4.57 [3.76–5.40], p = 0.010), whereas VWF antigen (VWF:Ag) was similar (respectively 0.34 IU/mL [0.28–0.39] vs. 0.34 [0.31–0.38], p = 0.644). DM + HC swine had no endothelial dysfunction or atherosclerosis during this short-term follow-up. Subsequently, we performed a long-term (15 months) longitudinal cohort study in 10 Landrace–Yorkshire swine, in five of which HC and in five combined DM + HC were induced. VWF:Ag was higher at 15 months compared with 9 months in HC (0.37 [0.32–0.42] vs. 0.27 [0.23–0.40], p = 0.042) and DM + HC (0.33 [0.32–0.37] vs. 0.25 [0.24–0.33], p = 0.042). Both long-term groups had endothelial dysfunction compared with controls and atherosclerosis after 15 months. In conclusion, short-term hyperglycemia and dyslipidemia increase FVIII, independent of VWF. Long-term DM and HC increase VWF via endothelial dysfunction and atherosclerosis. Therefore, VWF seems to be a biomarker for advanced cardiovascular disease.

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