Signs Of Endothelial Dysfunction Research Articles

Microalbuminuria as a Predictor of Early Neurological Deterioration and Poor Functional Outcomes in Acute Ischemic Stroke.

Background Ischemic stroke is a major health crisis with significant consequences. Microalbuminuria, a sign of endothelial dysfunction, has been linked to adverse outcomes in ischemic stroke. Early neurological deterioration (END) is a critical factor influencing the patient's prognosis. This study aimed to determine the prevalence of microalbuminuria, its predictive value in assessing END, and its prognostic implications in acute ischemic stroke (AIS). Methodology This study conducted at Pradyumna Bal Memorial Hospital, Kalinga Institute of Medical Sciences Bhubaneswar (November 2020-April 2022) included 114 AIS patients over 18 years who presented within 24 hours of stroke onset. Demographics, vascular risk factors, National Institutes of Health Stroke Scale (NIHSS) scores (admission and day three), modified Rankin scores (day 10), urinary albumin-to-creatinine ratios, and carotid artery Doppler studies were collected. Results The mean age of the patients was 61.87 years, with males constituting 72.8% of the population. Hypertension (50.9%) and diabetes mellitus (28.9%) were the most common comorbid conditions. The mean NIHSS stroke severity at presentation was 11.30. END occurred in 38.6% of patients. Overall, 43.9% of cases showed carotid stenosis, and the mean carotid intimal media thickness was 1.08 mm. Notably, the presence of microalbuminuria significantly increased the chances of both END (39.45 times higher risk) and worse functional outcomes (odds ratio = 19.147, p = 0.001). Conclusions Microalbuminuria emerges as a robust independent predictor of END and a poor prognosis in AIS. These findings highlight the importance of early microalbuminuria identification and intervention to reduce END risk and potentially improve outcomes in AIS patients.

Comparison of Blood Biomarkers in Systemic Blood and Varicose Veins: A Cross-sectional Study

Introduction: Varicose Veins (VV) are enlarged, convoluted, and elongated veins that primarily affect the superficial veins in the lower limbs and are one of the most prevalent indications of vascular diseases. The reasons for elevated venous pressure are understood, but the inflammatory cytokines that initiate the ultimate pathways of tissue destruction and are in charge of the clinical characteristics of Chronic Venous Insufficiency (CVI) are yet unknown. Although inflammation plays a crucial role in the process of tissue apoptosis, it also plays a crucial role in tissue repair and regeneration. Aim: To investigate changes in blood markers of varicose vein inflammation and endothelial damage and compare them with systemic markers in VV patients and conclude that they are increased in VV blood. Materials and Methods: The comparative cross-sectional study was conducted in the Department of Biochemistry on 70 patients with primary VV who were scheduled for Outpatient Sclerotherapy at Nootan Medical College and Research Centre, Sankalcahnd Patel Vidyadham in Visnagar, Gujarat, India from April 2021 to June 2023. Chronic lower extremity Venous Disease (CVD) was categorised using the Clinical Aetiology Anatomy Pathophysiology (CEAP) classification method. Blood samples were obtained above the knee from the tortuous and dilated varicose tributaries of the great saphenous vein (local) and from the antecubital (systemic) vein by standard venipuncture. Erythrocytes, leukocytes, platelets, haemoglobin, and haematocrit were determined using an automatic haematology analyser. D-dimer and High sensitivity C-reactive Protein (hsCRP) were determined by an immune turbidimetric assay. IL-6 and von Willebrand factor (vWF) were measured by Enzyme Linked Immunosorbent Assay (ELISA) using commercially available kits according to the manufacturers’ instructions. An Independent samples t-test was used to compare group difference, and p-value ≤0.05 were considered significant in all two-sided statistical tests. Results: Basic haematologic test results {systemic versus (vs) varicose blood samples} were comparable. In VV, the following parameters were significantly increased compared to systemic blood: Haemoglobin (12.85±1.81 g/dL vs. 15.82±1.57 g/ dL, p<0.001), hsCRP (1.34±1.01 mg/L vs. 3.78±1.67 mg/L, p<0.001), IL-6 (2.65±1.07 pg/mL vs. 4.17±1.51 pg/mL, p<0.001), vWF (90.73±16.72% vs. 127.30±19.92, p<0.001). D-dimer was also substantially higher in samples extracted from leg VV than in systemic blood (105.87±17.72 ng/mL vs. 85.61±18.18 ng/mL, p<0.001). Conclusion: Blood from VV has shown a higher level of several inflammatory markers and signs of endothelial dysfunction. This is most likely the result of worsening venous pressure and dilated, convoluted superficial veins that restrict blood flow. The procoagulant qualities of the local blood and damage to the venous wall, leading to a chronic inflammatory response, may accelerate the disease’s progression and thrombotic consequences.

Progesterone-induced blocking factor blockade causes hypertension in pregnant rats.

Preeclampsia (PE) is a multisystem disorder characterized by new onset hypertension in mid-late gestation and can include multi-organ dysfunction with or without proteinuria. It affects 5%-7% of all pregnancies in the U.S., making PE a major contributor to maternal and fetal morbidity and mortality. Currently, there is no cure for this pregnancy complication except for early delivery of the placenta and fetus. Moreover, the therapeutic options to treat PE are very limited. One potential trigger for the development of PE is progesterone deficiency-induced imbalance between T Helper 1(Th1)/Th2 cells, an increase in cytolytic natural killer (NK) cells and inflammatory cytokines that in turn leads to endothelial dysfunction, intrauterine growth restriction (IUGR) and hypertension. Importantly, progesterone signals the synthesis of progesterone-induced blocking factor (PIBF) which has anti-inflammatory effects and could promote the regulation of inflammation balance during pregnancy. However, the role of progesterone and PIBF in the pathophysiology of PE is still not fully understood. Thus, this current study was designed to test the hypothesis that inhibition of PIBF causes signs of PE in pregnant Sprague Dawley rats. In order to address our hypothesis, rabbit anti-PIBF IgG (0.25, low dose-LD or 0.50mg/mL, high dose-HD) was administered intraperitoneally on gestation day (GD) 15 to normal pregnant Sprague Dawley (NP) rats. On GD 18, carotid catheters were inserted and on GD 19 mean blood pressure (MAP) and samples were collected for further analysis. MAP in normal pregnant rats (NP) rats (n=7) was 99±3mmHg, which increased to 116±2 mmHg in NP+ anti-PIBF LD (n=10) and 113±4mmHg in NP+ anti-PIBF HD (n=4), p<0.05. Plasma TNF-alpha levels were 35±8 pg/mL in NP rats and increased to 84±21 pg/mL in NP+ Anti-PIBF HD (n=4), p<0.05. Plasma IL-4 and IL-10 levels were 22±5 and 25+6 pg/mL in NP (n=5), which decreased to 6±1 and 8±1 pg/mL in NP+ Anti-PIBF LD (n=6, p<0.05) and 16±4 and 15±5 pg/mL in NP+ Anti-PIBF HD (n=4). Circulating total NK cells were 67±11 % gatein NP rats (n=3), which decreased to 28±7% gate in NP+ Anti-PIBF LD and 45±6% gate in NP+ Anti-PIBF HD. Cytolytic NK cells were increased in NP+ Anti-PIBF HD, p<0.05. Moreover, circulating NO levels were significantly decreased while renal cortex PPET-1 levels increased NP+ Anti-PIBF HD. Our study demonstrates that PIBF blockade causes hypertension, inflammation and signs of endothelial dysfunction, all of which are associated with PE, thus indicating the importance of progesterone signalling pathways during a healthy pregnancy.

Relation between impaired coronary microvascular circulation and plasma atherogenic index in patients with ankylosing spondylitis

Aim: The coronary flow reserve (CFR) is a sign of endothelial dysfunction and early-stage coronary artery disease (CAD). Plasma atherogenic index (PAI) is related to subclinical CAD and may be used as a predictor of cardiovascular mortality. Our aim is to determine CFR and PAI in patients with AS and to investigate whether PAI can be used in the detection of early stage CAD.&#x0D; Methods: The study population comprised 48 patients, who were diagnosed with AS based on modified New York criteria and 35 healthy volunteers. PAI values were calculated with the formula log 10 triglyceride (TG) / high-density lipoprotein (HDL).&#x0D; Results: No difference was detected between the two groups for the demographic variables, including age, sex and BMI. The comparison of the groups for PAI and CFR demonstrated that PAI levels were observed to be significantly higher and CFR levels were observed to be significantly lower in the AS patients (p=0.01, p

The role of endothelial dysfunction, microcirculatory disorders, and hypoxia as mechanisms for the formation of lung lesions

In a review article, the authors consider the significance of endothelial dysfunction, microcirculation disorders, and hypoxia in the development of lung diseases and in the comorbid course of a number of other diseases of the internal organs. The role of endotheliocytes in the systemic response to inflammatory processes in the case of damage to the bronchopulmonary system is considered. Endothelial cells counteract pathogens in the blood and send signals warning of infection, invasion, or injury. The importance of the anticoagulant and antithrombotic properties of the endothelium (including the pulmonary one), which contribute to the fight against thrombosis, is emphasized. It is indicated that endothelial cells have an endogenous mechanism to combat platelet activation. This function depends on the surface expression of ecto-ATPase, CD39, and the release of nitric oxide and prostacyclin. Attention is paid to the importance of activation of the renin-angiotensin-aldosterone system both through angiotensin-II and through aldosterone. The authors stressed the importance of endothelial dysfunction as an imbalance between the factors of relaxation and constriction, coagulation, and fibrinolysis, which provide hemostasis of the main vital regulatory systems, and the stage of disease compensation (via the participation of nitric oxide). Microcirculation disorders and hypoxia are considered phenomena that are compatible in pathogenesis not only with pulmonary diseases but also as common comorbid syndromes with other diseases of the internal organs. This is explained by the fact that the common links are chronic oxidative stress, the reaction of the immune system to damage, the formation of a low-grade chronic systemic inflammation syndrome, a violation of the microcirculation process, and an increase in hypoxic and ischemic processes. The importance of knowledge about the mechanisms of development of endothelial dysfunction, microcirculation disorders, and hypoxia for therapeutic and rehabilitation tactics is emphasized.

Розлади ендотеліальної функції в дітей, які перехворіли на інфекцію COVID-19

Purpose - to learn the features of clinical condition and state of endothelial function as the marker of the development of cardiovascular pathology in children who suffered from COVID-19. Materials and methods. The research group consisted of 70 children aged 7-14 without chronic pathology who suffered from COVID-19 and had laboratory confirmation of the disease. Assessment of the functioning of the vessels’ endothelium was done by studying the dynamics of blood flow in the brachial artery and changes of it diameter at rest and during reactive hyperemia after an occlusion test. Statistical assessment of the obtained data was carried out by the application package «Statistica 10.0 for Windows» using the method of variational statistics. Student’s t-test was calculated to assess the reliability of mean values differences. Results. The state of endothelial function show that 85.4% of children after COVID-19 infection had signs of endothelial dysfunction, mainly hypoergic (32.9%) and paradoxical (30%) forms, while normoergic function of the endothelium was found only in 14.6% of children. In the same time in the group of children who did not suffer from COVID-19, was found that the normorergic form registrated in 80.0%, hyperergic endothelial dysfunction was found in 13.3% of children, and hypoergic - in 6.7% of children. Paradoxical endothelial dysfunction was not found in any child from this group. Conclusions. COVID-19 infection has negative consequences on the endothelium function and contributes to the development of endothelial dysfunction regardless of the severity of the disease course. Our results obtained the need of future study to develop an affordable and low-cost algorithm for routine use and identification of children with markers of lesion of cardiovascular system. 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 the participating institution. The informed consent of the patient was obtained for conducting the studies. No conflict of interests was declared by the authors.

Significance of Endothelial Dysfunction in Hypertensive Patients with Knee Osteoarthritis

Significance of Endothelial Dysfunction in Hypertensive Patients with Knee Osteoarthritis

Значение дисфункции эндотелия в патогенезе бруцеллеза

Значение дисфункции эндотелия в патогенезе бруцеллеза

CC16 ROLE IN BRONCHIOLITIS IN YOUNG CHILDREN

Introduction. CC16 protein is secreted by Club epithelial cells of the bronchioles, maintains homeostasis of theairway epithelium and has anti-inflammatory effects in the lungs. It is important to study the level of CC16 proteinin the serum in order to understand the integrity of the bronchial epithelium and the development of bronchialdysfunction in young children with bronchiolitis.Aim of the study. Analysis of blood serum CC16 concentration in younger bronchiolitis patients.Material and methods. We clinically examined 70 young children. The main group consisted of 35 non-allergicbronchiolitis patients. The comparison group included 25 young bronchiolitis patients with a history of allergies.The control group comprised 10 conditionally healthy children. The average age of patients was 8.4 ± 1.6 months,6.2 ± 1.4, and 6.4 ± 1.2 months in the main, comparison, and control group, accordingly. The complex of clinicaland-laboratory examination of children included CC16 serum tests. Serum CC16 content was determined by enzymelinked immunosorbent assay according to the “Human CC16 ELISA Kit”.Results of the study. It should be noted that the most main group patients (22 (62.8 ± 6.4%) of all examined) hadelevated CC16 readings. Whereas in the comparison group we did not find an increase in CC16 protein in any case.In contrast, 13 (51.8 ± 14.4%) children with bronchiolitis with a history of allergy had a decrease in CC16 protein,which may be a sign of endothelial dysfunction (p = 0.01).The study showed that young non-allergic bronchiolitis patients had the mean CC16 (38.9 ± 4.5 ng/ml) significantlyhigher than those with a history of allergies (22.9 ± 3.3 ng/ml), (OR=1,667; 0,854 - 3,250 95% CI; p &lt; 0,05). Thecontrol group patients had the mean CC16 within the reference interval (14.2 ± 2.12 ng/ml).Conclusions. In young children, elevated CC16 may be considered a marker of respiratory failure in bronchiolitispatients. Bronchiolitis patients with a history of allergies had statistically significantly lower serum CC16 levels thanthose in children without a history of allergies.

Features of cardiometabolic disorders in obesity on the example of the children’s population of the Rostov region

Objective: to study the features of the blood lipid profile in obese children and adolescents, depending on the presence of insulin resistance, endothelial dysfunction and minimal diastolic dysfunction of the left ventricle. Materials and methods: the study involved 370 obese children and adolescents from 7 to 17 years of age (the main group) with a body mass index BMI &gt; 30, the control group consisted of 123 children of the same age without obesity. Methods: clinical, paraclinical (biochemical blood test, blood pressure measurement, functional diagnosis of endothelial dysfunction, assessment of minimal diastolic dysfunction). Results: cardiometabolic disorders in obesity in childhood and adolescence are accompanied, first of all, by hypertriglyceridemia, which entails further violations of the lipid profile. There was also a positive correlation between changes in insulin and triglyceride levels in children and adolescents with obesity and endothelial dysfunction, as well as in patients with HOMA IR 3.2 and a combination of endothelial dysfunction and minimal dysfunction. Conclusions: based on the study of the nature of lipid spectrum disorders in obese children and adolescents and the presence of signs of endothelial dysfunction and/or minimal left ventricular dysfunction, it was concluded that obesity at this age is more often accompanied by minimal left ventricular diastolic dysfunction or a combination of endothelial dysfunction and left ventricular dysfunction. The development of insulin resistance leads to an increase in the combined pathology (ED and MDLj). Hypertriglyceridemia, which is associated with high levels of insulin and presumably determines the development of insulin resistance, plays an important role in the development of cardiometabolic disorders in obesity in childhood and adolescence.

Endothelial Dysfunction Diagnostic “Platform” in patients with diabetes mellitus

Objective: to determine the diagnostic signifi cance of endothelial dysfunction (ED) laboratory markers.Material and methods: we examined 276 men with type 2 diabetes mellitus (age 54.0[49;60] years). Patients underwent general clinical studies, analysis of carbohydrate and lipid metabolism parameters, adipohormones: leptin, resistin, adiponectin. Endothelial function was assessed by ultrasound examination of endothelium-dependent vasodilation (EDVD) of the brachial artery during a test with reactive hyperemia and determination of biochemical parameters of endothelial function — nitric oxide (NO), endothelial synthase NO type3, endothelin, ICAM-1, VCAM-1, p- and e-selectins, cadherin, PAI-1, VEGF-1, homocysteine B, C-reactive protein (CRP), osteoprotegerin. To assess the diagnostic signifi cance of the methods and to determine the cut-off , ROC analysis was used.Results: independent signifi cance in the diagnosis of ED was demonstrated by NO, ICAM-1, resistin (p&lt;0.001), CRP (p=0.006). Th e odds ratio of ED for resistin was 6.97, which is 1.9 times higher than NO and ICAM-1 and 3.7 times higher than CRP. Th e cut-off for diagnostic of ED are: NO — 97.3 μmol/L, ICAM-1 — 309.4 ng/ml, resistin — 6.32 ng/ml, CRP — 6.25 mg/L.Conclusion: the diagnostic platform for determining ED, along with the ultrasound assessment of EDVD, should include the analysis of its biochemical markers: NO, ICAM-1, resistin, CRP. Resistin is an independent, high-precision marker of ED, which is the pathogenetic link between endothelial dysfunction and adipose tissue dysmetabolism.

Endothelial TRPV4-eNOS coupling as a vital therapy target for treatment of hypertension.

Reduced NO levels and activity are signs of endothelial dysfunction, which is important in mediating BP changes. Previously, we demonstrated that transient receptor potential channel V4 (TRPV4) could form a functional complex with other proteins to mediate vasodilation in endothelial cells (ECs). But how TRPV4 interacts with the NO pathway in larger arteries requires further exploration. We used single-cell RNA-sequencing to find the CD106+ TRPV4high NOS3high ECs. The TRPV4-eNOS interaction was verified by co-immunoprecipitation and immuno-FRET, and their binding site was found by site-directed mutagenesis. Endothelium-specific TRPV4 knockout (TRPV4EC-/- ) mice were used to study the effect of the TRPV4-eNOS interaction on BP. A small molecule, JNc-463, was designed through molecular docking technology. We uncovered CD106+ TRPV4high NOS3high ECs in the mouse aorta, which could regulate vasodilation via a TRPV4-eNOS interaction, and were essential to regulate BP. The TRPV4-eNOS interaction markedly decreased during the process of hypertension. We further attempted to identify molecules involved in the TRPV4-eNOS interaction and developed a small-molecule drug, JNc-463, which could increase the TRPV4-eNOS interaction to enhance vasodilation and exert antihypertensive effects in mice. This is the first study integrating single-cell RNA-Seq, single-cell functional study and drug screening in aorta. We identified a subpopulation of CD106+ TRPV4high NOS3high ECs, in which an impaired TRPV4-eNOS interaction was important in the progress of hypertension, and we designed a small molecule, JNc-463, to improve the impaired TRPV4-eNOS interaction in hypertension.

Нарушения эндотелий-зависимой вазодилатации у больных с микрососудистой стенокардией

Background: disorders of both endothelium-dependent and endothelium-independent vasodilation play a role in the pathogenesis of microvascular angina (MVA), the contribution of which may be different. Aim: to study the processes of endothelium-dependent vasodilation (EDV) in patients with primary MVA. Patients and Methods: an open prospective study included 60 patients (mean age 57.3±6.4 years) with MVA, confirmed clinical picture (chest pain), coronary angiography data (the absence of coronary artery stenosis), positive stress test (pain syndrome and/or ST segment depression by ≥2 mm by treadmill exercise stress test), positron emission tomography (PET) myocardial perfusion imaging (MPI) with tests (cold pressor test and with adenosine). Patients with diseases that can lead to secondary microvascular dysfunction were not included in the study. To evaluate the processes of EDV, all patients underwent the following evaluations: peripheral arterial tonometry (PAT), assessment of circulating endothelial cells (CEC), high-sensitivity C-reactive protein (hsCRP), endothelin-1 (ET-1), total antioxidant status. Adding that, the results of a cold pressor test during PET were analyzed. Results: the majority of the examined patients were women — 81.7%. Most of the female patients included in the study (93.9%) were postmenopausal. In all patients with MVA, according to the data of PET MPI with cold pressor test, signs of EDV disorder were detected as a decrease in coronary blood flow through the three coronary arteries. During PET, the index of reactive hyperemia was reduced (&lt;1,67) in all examined patients and amounted to 1.43±0.15. According to the results of laboratory studies, there was an increase in the level of ET-1 and CEC — 3,335 [1,545; 3,952] fmol/L and 14±8 cells/3×105 leukocytes, respectively. The CRP level was 4,44 [1.02; 4.45] mg/L. The total antioxidant capacity was reduced in 53 (88%) patients, the average values of the indicator were 289,03±52,14 μmol/L. Conclusion: according to laboratory and instrumental studies, signs of endothelial dysfunction, namely disorders of EDV, were revealed in all examined patients with primary MVA. KEYWORDS: microvascular angina, peripheral arterial tonometry, endothelium-dependent vasodilation, positron emission tomography. FOR CITATION: Leonova I.A., Zakharova O.V., Boldueva S.A. Disorders of endothelium-dependent vasodilation in patients with microvascular angina. Russian Medical Inquiry. 2022;6(8):427–432 (in Russ.). DOI: 10.32364/2587-6821-2022-6-8-427-432.

Clinical and diagnostic significance of endothelial dysfunction and serotonin levels in children with hemolytic-uremic syndrome

Hemolytic-uremic syndrome is a serious problem in pediatrics and pediatric nephrology. Hemolytic-uremic syndrome is one of the leading causes of acute kidney injury with potential transformation into terminal chronic kidney disease. Currently, the endothelial dysfunction is strongly associated with changes in the serotonergic system in the pathogenesis of hemolytic-uremic syndrome. There are few studies that have revealed an increase in the blood plasma serotonin concentration in children with hemolytic-uremic syndrome, but its role in the pathogenesis of chronic kidney disease has been insufficiently studied. The progressive course of hemolytic-uremic syndrome, up to the terminal stage of renal failure, requires the search for markers of renal tissue damage as prognostically significant factors for the development of nephrosclerosis, which is of particular importance for optimizing the management of such children.

The pathogenetic significance of endothelial dysfunction in the development of diabetic nephropathy in patients with type 2 diabetes mellitus

Objective: to determine the level of circulating markers of endothelial dysfunction (endothelin‑1, von Willebrand factor (vfV), endothelial NO-synthase (e‑NOS)) in the blood serum of patients with type 2 diabetes mellitus (DM), as well as to assess the pathogenetic significance endothelial dysfunction in the development of diabetic nephropathy.Materials and methods: the study included 93 patients with type 2 DM, including 28 men (30.1%) and 65 women (69.9%), aged 30 to 79 years, the average age of patients was 59.7±8.4 of the year. The main group included patients with both newly diagnosed type 2 DM and a long-term diabetic history. The duration of the disease averaged 9.5±7.5 years. The majority of patients with DM type 2 (92.5%) at the time of inclusion in the study had various variants of microvascular complications of diabetes, only a small number of patientsin this group (7.5%) had no signs of diabetic angiopathy. Signs of various stages of diabetic nephropathy were observed in 60 patients (69.2%). The comparison group consisted of 30 patients with essential arterial hypertension, including 12 men (40%) and 18 women (60%), aged 34 to 70 years, on average 56.1 ± 8.1 years. The control group consisted of 32 apparently healthy individuals. In all patients, along with routine methods of clinical, laboratory and instrumental examination, the level of circulating markers of endothelial dysfunction (endothelin‑1, von Willebrand factor (vWF), endothelial NO-synthase (e‑NOS)) in blood serum was measured using enzyme-linked immunosorbent assay (ELISA).Results: in patients with DM type 2 and diabetic nephropathy, a statistically significant increase in the concentration of circulating markers of endothelial dysfunction was revealed in comparison with hypertensive patients and healthy individuals. An increase in the level of endothelin‑1 relative to the borderline reference value was found in 73 (78.5±4.1%), vfV in 63 (67.7±4.8%) and e‑NOS in 65 (69.9±4.7%) of patients with DM type 2. In the groups of participants with hypertension and healthy individuals, endothelial imbalance was noted by us significantly less often than in patients with DM type 2, the levels of endothelin‑1 and vfV in people with hypertension were increased in more cases than in healthy individuals. It was noted that the levels of circulating markers of endothelial dysfunction increase with an increase in the duration of DM type 2, and also significantly increase under conditions of carbohydrate decompensation.Conclusion: the results obtained confirm the pathogenetic role of endothelial dysfunction in the development of diabetic nephropathy in patients with type 2 diabetes, increasing endothelial imbalance in persons with a long diabetic history and lack of compensation for carbohydrate metabolism.

A Pilot Study: Hypertension, Endothelial Dysfunction and Retinal Microvasculature in Rheumatic Autoimmune Diseases.

Background: The etiology of autoimmune rheumatic diseases is unknown. Endothelial dysfunction and premature atherosclerosis are commonly seen in these patients. Atherosclerosis is considered one of the main causes of cardiovascular diseases. Hypertension is considered the most important traditional cardiovascular risk. This case-control study aimed to investigate the relationship between autoimmune diseases and cardiovascular risk. Methods: This study was carried out in patients with rheumatoid arthritis, RA (n = 10), primary Sjögren syndrome, PSS (n = 10), and healthy controls (n = 10). Mean blood pressure (MBP), systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse wave velocity (PWV, an indicator of arterial stiffness) were assessed via a Vicorder device. Asymmetric dimethylarginine (ADMA) was measured via ELISA. Retinal photos were taken via a CR-2 retinal camera, and retinal microvasculature analysis was carried out. T-tests were conducted to compare the disease and control groups. ANOVA and ANOVA—ANCOVA were also used for the correction of covariates. Results: A high prevalence of hypertension was seen in RA (80% of cases) and PSS (40% of cases) compared to controls (only 20% of cases). Significant changes were seen in MBP (RA 101 ± 11 mmHg; PSS 93 ± 10 mm Hg vs. controls 88 ± 7 mmHg, p = 0.010), SBP (148 ± 16 mmHg in RA vs. 135 ± 16 mmHg in PSS vs. 128 ± 11 mmHg in control group; p = 0.007), DBP (77 ± 8 mmHg in RA, 72 ± 8 mmHg in PSS vs. 67 ± 6 mmHg in control; p = 0.010 in RA compared to the controls). Patients with PSS showed no significant difference as compared to controls (MBP: p = 0.240, SBP: p = 0.340, DBP: p = 0.190). Increased plasma ADMA was seen in RA (0.45 ± 0.069 ng/mL) and PSS (0.43 ± 0.060 ng/mL) patients as compared to controls (0.38 ± 0.059 ng/mL). ADMA in RA vs. control was statistically significant (p = 0.022). However, no differences were seen in ADMA in PSS vs. controls. PWV and retinal microvasculature did not differ across the three groups. Conclusions: The prevalence of hypertension in our cohort was very high. Similarly, signs of endothelial dysfunction were seen in autoimmune rheumatic diseases. As hypertension and endothelial dysfunction are important contributing risk factors for cardiovascular diseases, the association of hypertension and endothelial dysfunction should be monitored closely in autoimmune diseases.

Clinical significance of expression of the marker of adaptation to hypoxia HIF-1α in pregnant women with initial forms of venous disease

Aim: to study the activity of the HIF-1á (hypoxia-inducible factor-1á) hypoxia marker in pregnant women with phlebopathy and its relationship with placenta morphological changes and perinatal complications.Materials and Methods. 70 women with phlebopathy were dynamically examined during pregnancy. The main group consisted of 30 patients with newborns showing signs of hypoxia; the control group consisted of 40 women with healthy children. All women underwent ultrasound examinations of the lower extremity veins and pelvis by assessing vascular patency, state of venous valves, and intensity of platelet sludge. Expression of the HIF-1á transcription factor at gestational age of 18–20 and 36 weeks was performed by using real-time polymerase chain reaction.Results. Altered functional state of the veins was found in all pregnant women from the main group, which was accompanied by formation of varying degree platelet sludge in the area of the venous valves in the majority of women, as well as signs of endothelial dysfunction and venous hypoxia highlighted with HIF1-á gene expression upregulated by 2.18-fold. No changes in such parameters were observed in control group.Conclusion. The transcription factor HIF1-á can be considered as a marker of unfavorable perinatal outcomes in pregnant women with signs of phlebopathy.

Ultrastructure of Endothelial Cells of Myocardial Capillaries in Burn Septicotoxemia.

We studied ultrastructure and vesicular structures in endothelial cells of myocardial micro-vessels in burn patients. Electron microscopy revealed a significant decrease in volume density of vesicular structures in the endotheliocytes of myocardial capillaries in patients with burn septicotoxemia. The observed structural signs of endothelial dysfunction revealed in this category of patients can be a promising area for further research and for the development of methods of pathogenetic correction of myocardial disorders in the case of burn injury.

To Study the Frequency of Albuminuria in Diabetics Brought in with Stroke: A survey at Tertiary Care Hospital

Background: Albuminuria is thought to be a separate risk factor for stroke. A strong association between diabetes related albuminuria and stroke has been published in the international literature. Albuminuria being a sign of endothelial dysfunction, atherosclerosis is a strong predictor of strokes. Aim: To investigate the albuminuria as a predictor of stroke in diabetics in our population. Study design: Observational study. Place and duration of study: This study was done in the Department of Neurology, Sharif Medical &amp; Dental College/Hospital, Lahore from January to August 2019. Methodology: One hundred and fifty diabetic patients having ages 25 to 75 years presented with stroke were enrolled in this study. Demographics (age, sex, residence and socio-economic status) of the included population and types of stroke were recorded on study proforma after getting brain CT of each patient. Urine for albuminuria was examined under microscope. Results: In this study (63%) were males and 37% were females with M:F ratio 2.54:1. Major portion of the patients (43%) were ages between 25-45 years mean±SD 51.62±8.45. Ischemic stroke was found in 114 (76%) hemorrhagic in 24(16%) and undetermined in 12(8%) patients respectively. Albuminuria was found in 72(48%) patients, Group A 40(69%) had ischemic stroke, 10(17%) had hemorrhagic and 8(14%) had undetermined stroke. Conclusion: It is concluded that is strong relation between microvascular complications with macrovascular complication of diabetes (i.e. albuminuria with stroke). The stoke patients with diabetes has more frequency of albuminuria as compared to non diabetics. Keywords: Albuminuria, T2DM, Stroke, Hemorrhagic.

H2S-ВИВІЛЬНЮЮЧИЙ НЕСТЕРОЇДНИЙ ПРОТИЗАПАЛЬНИЙ ПРЕПАРАТ АТВ-340 ЗНИЖУЄ МЕЗЕНТЕРІАЛЬНОГО МЕТАЗАПАЛЕННЯ ЗА УМОВ СТАРІННЯ ТА ПОШКОДЖУВАЛЬНОГО ВПЛИВУ ВИСОКОФРУКТОЗНОЇ ДІЄТИ

Metaflammation (MF) is associated with visceral adiposities involved in the metabolic, cardiovascular, and gastrointestinal disease pathogenesis while their target therapeutic strategy is still limited. The link between mesenteric white adipocytes (MA) and stromal-vascular cellular remodeling in advanced age and Western diet consumption which is the base of MF remain undiscovered. Hydrogen Sulfide (H2S) non-steroidal anti-inflammatory drugs (H2S-NSAIDs) are a promising novel class of drugs regarding their cytoprotective, regulatory redox signaling, vasodilatory, and anti-inflammatory effects. Aim. To study the effectiveness of novel H2S-NSAIDs ATB-340, a hybrid compound of H2S and aspirin (ASA) over conventional ASA, and combination of ASA and NaHS on mesenteric cellular adaptive changes in experimental age- and high fructose dietary (HFD)-induced injury. Methods: Mesenteric subcellular adaptive responses of aged male rats on a standard diet (SD) or 4 weeks HFD that underwent acute water-immersion restraint stress (WIRS) were evaluated by electron microscopy. The effects of 9 days exogenous administration of ATB-340 (17.5 mg/kg/day), ASA (10 mg/kg/day) and sodium hydrosulfide (NaHS, 5.6 mg/kg/day) were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), thiosulfate-dithiol sulfurtransferase (TST), and sulfite oxidase (SO) were examined biochemically using spectrophotometry. Results: In HFD groups exposed to WIRS treatment with ATB-340 protected MA, as well their mitochondria, microvascular endothelial, and sub-endothelial structures, fibroblasts were observed vs the ASA and H2S+ASA-treated groups that had signs of endothelial dysfunction, MA damage with dysfunctional mitochondria, and mitochondria with fat incorporation. In rats fed with HFD and ASA treatment, low activities of CSE, CBS, TST and the rise of TBARS level and SO activity were observed. Treatment with ASA+NaHS, ATB-340 of aged rats lowered TBARS and enhanced H2S enzyme activities in contrast to the vehicle-treated group (p &lt; 0.05). Conclusions. Mitochondrial alterations, endothelial damage, and redox disbalance are key factors for aged rat mesenteric adipose tissue remodeling during Western diet consumption. Our results contributing to identifying powerful intervention by effective compound H2S-ASA, novel H2S-NSAIDs, which has the potential to modulate mesenteric metaflammation, vascular function by enhancement H2S synthesis and redox regulatory and cytoprotective activities