scholarly journals THE STRUCTURAL FEATURES OF VASCULAR ENDOTHELIUM IN ACUTE CEREBRAL ISCHEMIA

2017 ◽  
Vol 3 ◽  
pp. 32-37
Author(s):  
Anna Kosheleva

The aim of the research was to study the number and structural properties of desquamated endothelial cells (DECs) in the peripheral blood in carotid ischemic stroke (CIS) and carotid transient ischemic attacks (TIAs) and its connection with the marker of endothelial dysfunction - endothelin-1. We examined 35 patients with the first CIS, on days 1st and 10th, and also 34 patients with symptomatic carotid TIAs, on days 1st and 10th of the observation. Middle age of the examined patients with a CIS was 63,7±1,0. Middle age of the examined patients with the ТIАs was 54,7±1,0. 25 practically healthy persons were examined as a group of control. Neurologic deficit was assessed with the National Institutes of Health Stroke Scale (NIHSS). DECs were estimated by CD34 immunobead capture in the peripheral venous blood of patients and persons of control group. We studied the level of endothelin-1 in the peripheral venous blood of patients and persons of control group using the enzyme immunoassay using the Biomedica (Austria) during the first 24 hrs and on day 10. Statistical processing of the obtained results was carried out using statistical analysis package Statistica. In this case, the mean value, the standard error and the correlation analysis were determined. Samples were compared using the Student's criterion (t) and the correlation coefficient (r). During an examination of 35 patients in the acute period of CIS and 34 patients with carotid TIAs using the immunocytochemical method the number of DECs was studied in venous blood. The quantitative analysis of vascular endothelium in acute cerebral ischemias showed its statistically unreliable differences in CIS and TIAs. A conclusion is drawn about the general mechanisms of endothelial dysfunction in CIS and TIAs. The number of DECs significantly correlates with the terms of disease. Regress of this indicator is noted in patients by the end of follow-up in both observation groups. During the first 24 hrs in patients with CIS and TIAs density of DECs of blood directly correlates with the level of endothelin-1 blood. The endothelin-1 level tends to decrease by the 10th day of observation and the correlation force with the DECs level is correspondingly reduced.

2010 ◽  
Vol 37 (4) ◽  
pp. 711-716 ◽  
Author(s):  
WILL FOSTER ◽  
DAVID CARRUTHERS ◽  
GREGORY Y.H. LIP ◽  
ANDREW D. BLANN

Objective.To determine whether abnormalities in microvascular and macrovascular function in rheumatoid arthritis (RA) are associated with plasma markers [von Willebrand factor (VWF)] of endothelial dysfunction and inflammation [C-reactive protein (CRP)] and whether the abnormalities would be altered by treatment. Endothelial dysfunction and inflammation in RA may contribute to adverse cardiovascular events. Although endothelial dysfunction in RA has been demonstrated by altered plasma markers, the relationships with macrovascular and microvascular function are relatively unexplored.Methods.We recruited 66 patients with chronic RA, 48 community controls (CC), and 25 patients with diabetes and hypertension as a disease control group (DC). Subjects had venous blood sampled for plasma markers, and underwent laser Doppler perfusion imaging of forearm skin (to assess microvascular circulation) following acetylcholine and sodium nitroprusside iontophoresis, to assess endothelium-dependent and endothelium-independent responses, respectively. Brachial artery flow-mediated dilatation assessed endothelial dysfunction in a macrovascular bed. A subgroup of 29 patients with RA were assessed pretherapy and after 2–4 weeks of antirheumatic therapy.Results.As expected, patients with RA had higher CRP, erythrocyte sedimentation rate (ESR), and VWF. Endothelium-independent vasoreactivity was abnormal in RA, and this correlated negatively with CRP. All aspects of microvascular function were abnormal in the DC compared to the CC. Macrovascular function was preserved in RA but was abnormal in the DC group. Four weeks of antiinflammatory therapy reduced CRP and ESR but had no effect on any vascular function index in the patients with RA.Conclusion.Patients with RA have abnormal endothelium-independent microvascular function that correlates with inflammation but is not altered by short-term antiinflammatory therapy.


2020 ◽  
pp. 528-534
Author(s):  
A. M. SABUROVA ◽  
◽  
KH.R. NASYRDZHANOVA ◽  
KH.YO. SHARIPOVA ◽  
◽  
...  

Objective: Examination the relationship between the state of biomembranes and indicators of endothelial dysfunction in patients with chronic obstructive pulmonary disease (COPD). Methods: 40 patients with COPD at the age of 27-64 years were treated at the City Health Center № 2 named after academician K.T. Tadzhiev. There were 21 men (52.5%), and 19 women (47.5%). The control group is represented by 30 healthy persons, comparable by sex and age. The content of inflammatory markers of vascular endothelium – CRP, fibrinogen and von Willebrand factor (VWF) – was studied. The functional state of erythrocyte membranes was studied by determining of permeability of erythrocyte membranes (PEM) and sorption ability of erythrocytes (SAE). Results: Study of endothelial dysfunction in patients with COPD showed an increase in fibrinogen content by 71.15% (2.6±0.08 and 4.45±0.16 g/L), VWF by 35.4% (95.7±2.3 and 129.6±2.3%) and an increase in serum CRP by 15 times (2.09±0.1 and 32.2±0.1 mg/L). There was a change in PEM and an increase in SAE by 27.8% (39.5±0.5 and 50.5±0.6%, respectively) compared with the control group, that reflects damage of erythrocytes and is considered as a factor of endogenous intoxication. A significant direct relationship was established between SAE and indicators of vascular dysfunction: with VWF (r=0.34; p<0.05) and fibrinogen (r=0.47; p<0.05). Conclusions: The development and progression of COPD are accompanied by dysfunction of the vascular endothelium, the criteria for which are an increase in the level of CRP, fibrinogen and VWF. On the background of COPD, erythrocytes are involved in the pathological process, which is confirmed by an increase in PEM and SAE and with a significant relationship between SAE and endothelial dysfunction. Laboratory manifestations of endothelial dysfunction accompanied by functional impairment of biomembranes (increased PEM and increased SAE), can be considered as a factor of the poor prognosis of COPD. Keywords: COPD , biomembrane, endothelial dysfunction, CRP, fibrinogen, von Willebrand factor, permeability of erythrocyte membranes, sorption ability of erythrocytes.


2018 ◽  
Vol 24 (4) ◽  
Author(s):  
Natalya Drohomyretska ◽  
Natalya Henyk

The objective of the work: to study the changes of the functional activity of the endothelium and the plasma-coagulation link of hemostasis in women with chronic inflammatory processes of the internal genital organs (CIPIGO) with and without varicose veins of the small pelvis (VVSP).Materials and methods: 68 women with chronic inflammatory processes of the internal genital organs against the background of varicose veins of the small pelvis (group 1); 52 women with chronic inflammatory processes of the pelvic organs without varicose veins of the small pelvis (group 2); 30 practically healthy women (control group) were examined before and after the treatment. The age of women was between 18 and 45 years old. All the patients of the study groups received the treatment offered by us, which included a diosmine-containing phlebotropic preparation normoven, 500 mg twice a day in continuous mode and a donor of nitric oxide tivortin aspartatum, 5 ml 3 times per os for 14 days each month during six months.Determination of concentration of endothelin-1, prostacyclin was performed by immunoassay using a set of reagents from the firm “Biomediсa” (Austria); the determination of D-dimers in blood plasma was performed by latex-test of the firm “Organon-Tekhnika”.Results of workIn women with CIPIGO with and without VVSP, the increased production of endothelin-1, which has a pro-aggregate and pro-inflammatory effect, was determined. At the same time, the decrease of the synthesis of prostacyclin, which has anti-aggregant properties, was noted. In evaluating the indicators of coagulograms in patients of the studied groups, the propensity for hypercoagulation was revealed, as evidenced by an increase in the level of fibrinogen and a rise of index of the phospholipid-dependent coagulation tests. The decrease of the percentage of fibrinolytic blood activity and the increase in plasma concentration of the molecular marker of thrombophilia D-dimer can be considered as activation of intravascular coagulopathy and the presence of endothelial dysfunction.Conclusions: 1. Our studies found endothelial dysfunction and violations of the plasma-coagulation linkage of hemostasis in both studied groups. 2. After the performed treatment, the improvement of the functional activity of the endothelium and normalization of the main parameters of the plasma-coagulation linkage of hemostasis were observed.


Medicina ◽  
2008 ◽  
Vol 44 (3) ◽  
pp. 201 ◽  
Author(s):  
Algimantas Šurna ◽  
Jurgina Sakalauskienė ◽  
Astra Vitkauskienė ◽  
Viktoras Šaferis

Objective. To investigate bacterial populations in subgingival and supragingival plaque samples of patients with inflammatory periodontal diseases and activities of the lysosomal enzymes – lysozyme, alkaline phosphatase, and b-glucuronidase – in peripheral venous blood, in gingival crevicular fluid, and mixed nonstimulated saliva. Methods and materials. The study included 60 patients with inflammatory periodontal diseases without any internal pathology and 24 periodontally healthy subjects. Molecular genetic assay (Micro-IDent plus, Germany) for complex identification of additional six periodontopathic bacteria was applied. The activity of lysozyme was determined turbidimetrically, the activity of alkaline phosphatase – spectrophotometrically with a “Monarch” biochemical analyzer, the activity b-glucuronidase – according to the method described by Mead et al. and modified by Strachunskii. Results. A statistically significant association between clinical and bacteriological data was found in the following cases: gingival bleeding in the presence of Eubacterium nodatum, Eikenella corrodens, Capnocytophaga spp. (P<0.01); pathological periodontal pockets in the presence of Peptostreptococcus micros (α≤0.05 and β≤0.2), Fusobacterium nucleatum (α≤0.05 and β≤0.2), Campylobacter rectus (α≤0.05 and β≤0.2), and Capnocytophaga spp. (P<0.05); and satisfactory oral hygiene in the presence of all microorganisms investigated (P<0.05). The activity of lysozyme in gingival crevicular fluid and mixed nonstimulated saliva indicates the severity of periodontal inflammation. Based on clinical data, in assessing the amount of lysozyme in mixed nonstimulated saliva, sensitivity and specificity of 100% was found. Increased activities of lysozyme, alkaline phosphatase, and b-glucuronidase were found in peripheral venous blood of patients with inflammatory periodontal disease as compared to control group. Conclusions. The main principles of the treatment of periodontal inflammatory diseases should be based on microorganism elimination, creation of individual treatment means affecting microflora in the mouth and immune system of macroorganisms.


Issues related to the diagnosis and treatment of irritable bowel syndrome occupy one of the central places in gastroenterology, due to the fact that in recent years there has been a significant increase in the incidence of this syndrome, its long-term recurrent, often lifelong course, leading to a decrease in the performance of patients, despite good quality, and a significant cost to the health care system. Irritable bowel syndrome, despite its functional nature, occurs quite often - from 14-50% of the adult population according to population epidemiological studies, and the ratio of women to men is from 2: 1 to 4:1. In the structure of gastroenterological pathology, this disease accounts for 40-70% of all cases of seeking medical help. Irritable bowel syndrome is a complex of functional disorders of the distal intestines, lasting more than 3 months and accompanied by abdominal pain that disappears after a bowel movement, flatulence, a feeling of incomplete bowel movement, changes in the frequency and consistency of stools. Factors in the pathogenesis of irritable bowel syndrome are dysfunction of mental activity with changes in autonomic and humoral functions; visceral hypersensitivity and impaired intestinal motility, past intestinal infection; endocrine disorders; food allergies, sedentary lifestyle; genetic predisposition. Endothelial dysfunction has recently played an important role in the onset of irritable bowel syndrome. The most famous among the factors of vascular endothelium today are the powerful vasoconstrictor endothelin-1 and the vasodilator - nitric oxide. The study investigated the level of vasoconstrictor endothelin-1 and vasodilator of nitric oxide in patients with irritable bowel syndrome with constipation. It was found that such patients have severe endothelial dysfunction, which manifests itself in an increase in the level of endothelin-1 (р˂0,01), a decrease in the level of nitric oxide (р˂0,01). The data obtained indicate the role of dysfunction of the vascular endothelium in the pathogenesis of irritable bowel syndrome with constipation. An inverse correlation was found between the content of endothelin-1 and nitric oxide (p˂0.01), which indicates an increase in the activity of vasoconstrictor mechanisms with a simultaneous decrease in vasodilation factors. The effectiveness of complex therapy in the group of patients in whom folic acid and zincteral were used as part of complex therapy in improving the clinical picture of the disease (complete relief of dyspeptic syndrome and a significant decrease in the severity of pain, constipation and asthenic syndromes), restoration of vascular endothelial function (significant decrease in the level of endothelin-1 and an increase in the level of nitric oxide) in comparison with the group of patients in the treatment of which only basic therapy was used.


2019 ◽  
Vol 72 (4) ◽  
pp. 568-574
Author(s):  
Ylia O. Smiianova ◽  
Ludmyla N. Pristupa ◽  
Viktoriia Yu. Harbuzova ◽  
Yelizaveta A. Harbuzova

Introduction: Arterial hypertension is a multifactorial disease developing under the influence of environmental factors and is genetically determined. One of the genetic markers that is of primary importance in the disease development is endothelin-1 gene (EDN1). Today the association between the polymorphic variants of this gene, particularly Lys198Asn-polymorphism, and the development of arterial hypertension in different populations of the world has been proved. The aim: To study the association between the Lys198Asn-polymorphism of the endothelin-1 gene and the development of arterial hypertension in Ukrainian population. Materials and methods: The genotypes were determined by the polymerase chain reaction method, followed by the analysis of the restriction fragment length (PCR-RFLP) in venous blood of 160 patients with arterial hypertension and 110 people in the control group. The statistical analysis was performed using SPSS-17.0. Results: As a result of genotyping, it was found that in the group of patients with arterial hypertension the ratio of homozygote of the major allele (Lys/Lys), heterozygote (Lys/Asn) and homozygote of the minor allele (Asn/Asn) was 74 (46.3%), 73 ( 45.6%), 13 (8.1%), while in control - 66 (60.0%), 41 (37.3%), 3 (2.7%) respectively. The distribution of genotypes in the experimental groups was statistically significant (χ2 = 6.66; P = 0.036). By the method of binary logistic regression within the dominant and additive model of inheritance, a reliableassociation between the genotype of the Lys198Asn-polymorphism of the ET-1 gene and the development of arterial hypertension was established. It was shown that carriers of minor allele (Lys/Asn+Asn/Asn) have a risk of arterial hypertension 1.7 (95 % CI = 1.066 – 2.851), and homozygotes Asn/Asn 3.9 (95 % CI = 1.016 – 9.566)times higher than people with Lys/Lys genotype. In addition, smoking patients with Lys/Asn and Asn/Asn- genotypes have a risk of arterial hypertension 2.6 (95% of SI = 1.224-5.488), and homozygotes of the minor allele (Asn/Asn) 7.3(95% of SI = 1.295-41.639) times higher than the Lys/Lys homozygotes. Conclusions: Lys198Asn-polymorphism of the endothelin-1 gene is associated with the development of arterial hypertension in Ukrainian population. Carriers of minor allele (Lys/Asn+Asn/Asn) have a risk of arterial hypertension 1.7, and homozygotes Asn/Asn 3.9 times higher than people with Lys/Lys genotype.


2010 ◽  
Vol 298 (2) ◽  
pp. H340-H345 ◽  
Author(s):  
Tommaso Gori ◽  
Saverio Dragoni ◽  
Giuseppe Di Stolfo ◽  
Silvia Sicuro ◽  
Andrew Liuni ◽  
...  

Damage and dysfunction of the vascular endothelium critically influence clinical outcomes after ischemia and reperfusion (I/R). Brief exposure to organic nitrates can protect the vascular endothelium from I/R injury via a mechanism that is similar to ischemic preconditioning and is independent of hemodynamic changes. The clinical relevance of these protective effects clearly depends on whether they can be sustained over time. Twenty-four healthy (age 25–32) male volunteers were randomized to receive 1) transdermal nitroglycerin (GTN; 0.6 mg/h) administered for 2 h on 1 day only, 2) transdermal GTN for 2 h/day for 7 days, or 3) continuous therapy with transdermal GTN for 7 days. Eight volunteers underwent continuous GTN therapy followed by intra-arterial infusion of the antioxidant vitamin C. Finally, five additional subjects underwent no therapy and served as controls. Endothelial function measurements were performed before and after induction of I/R of the arm. I/R caused a significant blunting of the flow responses to acetylcholine in the control group ( P < 0.01 vs. before I/R). A single 2-h GTN dosage, given 24 h before I/R, prevented I/R-induced endothelial dysfunction [ P = not significant (NS) vs. before I/R], but this protective effect was completely lost after 1 wk of GTN administration 2 h/day ( P < 0.05 vs. before I/R; P = NS vs. control). In subjects who received continuous GTN, endothelial responses were blunted before I/R, and I/R did not cause further endothelial dysfunction. Finally, vitamin C normalized acetylcholine responses and prevented the loss of preconditioning associated with prolonged GTN. In a separate experimental model using isolated human endothelial cells, short-term incubation with GTN caused upregulation of heme oxygenase, an effect that was lost after prolonged GTN administration. Although a single administration of GTN is able to protect the endothelium from I/R-induced endothelial dysfunction, this protection is lost upon prolonged exposure, likely via an oxidative mechanism.


2018 ◽  
Vol 15 (1) ◽  
pp. 32-37
Author(s):  
S A Babanov ◽  
R A Baraeva ◽  
D S Budash ◽  
A G Baykova

A complete physical examination of 145 patients with various forms of hand-arm vibration syndrome (HAVS) and 30 patients of control group was performed in order to solve the aims and objectives of the research. The HAVS forms included 1st stage HAVS associated with local vibration, 2nd stage HAVS associated with local vibration, 2nd stage HAVS associated with local vibration comorbid with hypertension, 1st stage HAVS associated with general vibration, 2nd stage HAVS associated with general vibration, 2nd stage HAVS associated with general vibration comorbid with hypertension. It was observed that endothelial dysfunction in HAVS, especially when comorbid with hypertension, is accompanied by immune alterations such as humoral immunity factors and cytokines imbalance and is characterized by pro-inflammatory cytokine levels increase (IL -1β, IL -8, TNF-α) and anti-inflammatory cytokine level decrease (IL-4) from exposure to production vibration regardless of its type especially when comorbid with hypertension. It is proven that in isolated HAVS associated with local or general vibration, especially when comorbid with hypertension, endothelial dysfunction is characterized by increase of endothelin-1 serum level and growth factors such as transforming growth factor β1 (TGF-β1) and vascular endothelial growth factor А (VEGF-A) increase. Increase of endothelin-1 serum level in patients with HAVS is associated with hemostatic alterations such as platelet-derived growth factor ВВ (PDGF-BB), fibronectin, and Willebrand factor increase.


2015 ◽  
Vol 70 (5) ◽  
pp. 599-603 ◽  
Author(s):  
O. N. Sergeeva ◽  
N. P. Chesnokova ◽  
E. V. Ponukalina ◽  
I. E. Rogozhina ◽  
T. N. Glukhova

Until now, there is no systematic information on the role of endothelial dysfunction in the mechanisms of disorders of blood coagulation potential and microcirculation in different organs and tissues in preeclampsia.Objective: Our aim was to extend the existing principles of diagnosis of pre-eclampsia by establishing the role of endothelial dysfunction in the mechanisms of blood coagulation potential violations. Methods: A prospective comparative study was performed. Condition of coagulation processes studied by conventional techniques, parameters of a functional endothelium (nitric oxide metabolites, endothelin 1, thrombospondin, thrombomodulin and intercellular adhesion molecules in blood plasma) — by ELISA.Results: The study group included 55 patients with moderate preeclampsia and 49 pregnant women with severe pre-eclampsia, in the control group — 40 women with physiological pregnancy. In patients with pre-eclampsia moderate observed increase in plasma endothelin-1 (p 0.001), thrombospondin (p 0.001), intercellular adhesion molecules (p 0.001) while reducing the level of nitrogen oxide (p 0.001), increase in time of fibrinolysis (p 0.050) and decreased international normalized ratio (p 0.050) compared with the control group. With increasing severity of preeclampsia the researchers detected in blood plasma of patients a progressive increase in endothelin 1 (p1 0.020), thrombospondin (p1 0.001), intercellular adhesion molecules (p1 0.001) and decrease of nitric oxide metabolites (p1 0.001) and thrombomodulin (p1 0.001); the last combined with the activation of procoagulant hemostasis.Conclusion: There is a pathogenetic relationship between the development of endothelial dysfunction, impaired blood coagulation potential and the severity of clinical signs of preeclampsia. To widen the number of existing techniques to diagnose the severity of pre-eclampsia we recommende to mesure endothelin 1, thrombomodulin, thrombospondin, intercellular adhesion molecules and nitric oxide metabolites in the blood plasma, and use traditional indicators to assess the hemostatic system.


Author(s):  
PETR P. SHCHETININ ◽  
VERA I. SMOL’YAKOVA ◽  
TATYANA M. PLOTNIKOVA ◽  
ALEKSANDR V. KUCHIN ◽  
AleksandrVLADIMIR V. UDUT

Objective: Our research focuses on the endothelial protective effects of 2,6-diisobornyl-4-methylphenol. Its effect was revealed while studying rats experiencing myocardial ischemia/reperfusion. The research results demonstrated that there are significant disturbances in the vascular endothelium manifested by a decrease in the vasodilating activity and antiplatelet properties of 2,6-diisobornyl-4-methylphenol. Methods: We designed our own model of myocardial ischemia/reperfusion and applied it to 52 adult outbred Wistar males. We employed some methods of hemostasiological research such as thromboelastography to determine the antiplatelet activity of the vascular wall, G. Born nephelometric method to study platelet aggregation, phase contrast microscopy to count platelet counts in blood plasma, measurement of intra-arterial pressure to study the endothelial vasodilating function, and calculated the endothelial dysfunction coefficient in rats. Results: Preventive intragastric injection of 2,6-diisobornyl-4-methylphenol (100 mg/kg, 3 days before and 5 days after reproducing the myocardial ischemia/reperfusion model) increased the antiplatelet activity of the vascular endothelium in rats by 37% compared to the endothelium of the abdominal aorta segment of untreated animals. Moreover, 2,6-diisobornyl-4-methylphenol decreased the endothelial dysfunction coefficient by 43% in comparison with the value in the control group. Conclusion: 2,6-diisobornyl-4-methylphenol has an endothelial protective effect proved by its ability to increase antiplatelet properties of the endothelium and decrease the endothelial dysfunction coefficient. The revealed endothelial protective properties of 2,6-diisobornyl-4-methylphenol can be regarded as one of the potential mechanisms of cardioprotective activity of the drug.


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