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Biomedical subjects

N Iu Nikolaeva

Publications and source records attributed to N Iu Nikolaeva.

At least 19 recordsLinked to original sources
PubMed2005

[Effect of mexicor on oxidative stress in acute myocardial infarction].

Mexicor (5% solution and capsules) was used in 40 of 80 conventionally treated patients with acute myocardial infarction. The drug was given intravenously for 5 days, than intramuscularly (6-9 mg/kg) for 9 days and orally (0.1 mg t.i.d.) thereafter until discharge. Severity of oxidative stress was evaluated by K coefficient. Calculation of this coefficient required data on degree of oxidation of lipids in blood serum, serum levels of diene conjugates, malonic dialdehyde, alpha-tocopherol and ceruloplasmin. These parameters as well as activity of superoxide dismutase, glutathione peroxidase and catalase in erythrocytes were measured at admission, on days 2, 3, 7, 14 and at discharge. Mexicor treated compared with untreated (n=40) patients were characterized by diminished severity of oxidative stress at the account of lower levels of lipid peroxidation products and augmented compensatory potential of the endogenous antioxidant system.

Administration, Oral↗
PubMed2004

[Analysis of nitrites and nitrates (Unox) in urine].

Nitrite (NO2) and nitrate (NO3) concentrations are usually measured as a marker of NO metabolism. The aim of this study was to validate and standardize a method for the quantification of these two metabolites (nitrite and nitrate) in urine. The sample (urine) were deproteinized with NaOH, zinc sulfate and reduced with cadmium granules. Analytical recovery of NO3 added to urine samples after reduction with cadmium granules was 96-105% (Griess reaction). Calibration curves for nitrite and nitrate were linear over the concentration range of 2.1 to 200 micromole/L in urine. The detection limit of the assay was 0.9 micromole/L and the quantification limit was 2.1 micromole/L. Usual values were determined for healthy subjects: the mean concentration of NO2/NO3 (Unox) was 51.1 +/- 5.3 micromole/mmol creatinine (mean +/- SEM) (n = 15). Within-run precision was 6.6% and between-day precision was 2.2%.

Cadmium↗
PubMed2004

[The nature of a relationship of nitric oxide with angiotensin-converting enzyme and malonic dialdehyde in patients with atherogenic stenosis of the internal carotid artery].

In patients with stenosis of the internal carotid artery (ICA), a relationship was studied between the level of nitric oxide (NO) and the activity of angiotensin-conversing enzyme (ACE) and malonic dialdehyde (MDA) in the blood serum taken from: 1) the cubital vein an hour before carotid endarterectomy; 2) ICA before surgery; 3) the internal jugular vein before surgery; 4) ICA 5 min after surgery; 5) the internal jugular vein 5 min after surgery; 6) the cubital vein an hour following surgery. There was a direct correlation between the level of NO and the activity of ACE and an inverse correlation between the content of NO and MDA in the sera taken from the cubital, internal jugular vein, and ICA before and after endarterectomy. There were significant increases in the level of NO, in the activity of ACE, and in the content of MDA and total cholesterol in the serum taken from the cubital vein before carotid endarterectomy, which is indicative of significant oxidative stress and the necessity of its pathogenetic correction.

Aged↗
PubMed2003

[Leukocytic and thrombocytic generation of nitric oxide in patients with bronchial asthma].

Leukocytic and thrombocytic nitric oxide generation was studied in 23 healthy individuals and 17 patients with bronchial asthma. Differential centrifugation was used to isolate leukocytes and platelets from blood. The suspensions of leukocytes (5.10(6)) and platelets (0.5.10(8)) were incubated in 0.5 ml of the medium RPMI 1640 at 37 degrees C for 15 hours. The concentration of the stable metabolite of NO nitrite was estimated by the Griss test. The relative leukocytic NO production was 0.75 +/- 0.06 and 1.32 +/- 0.06 mumole/l in healthy individuals and patients, respectively (p < 0.001). The relative thrombocytic NO production was 2.15 +/- 0.14 and 2.26 +/- 0.07 mumole/l in healthy individuals and patients, respectively. The absolute leukocytic NO production was 0.47 +/- 0.05 and 0.65 +/- 0.05 mumol/l in healthy individuals and patients, respectively (p < 0.01). The absolute thrombocytic NO production was 7.70 +/- 0.55 and 5.32 +/- 0.27 mumole/l in healthy individuals and patients, respectively (p < 0.001). Therefore, the absolute production of NO by platelets is 16 times higher than that by leukocytes. In the patients, the relative and absolute leukocytic NO productions increased and the absolute thrombocytic NO production significantly decreased.

Adult↗
PubMed2003

[Generation of nitric oxide by peripheral blood leukocytes and platelets in thoracic and abdominal wounds].

Generation of nitric oxide (NO) by human blood leukocytes and platelets was studied in 23 healthy persons and in 22 patients with thoracic and abdominal wounds. The sum of points ranged, in victims, from 12 to 19 according to the APACHE II severity-degree condition. Leukocytes and blood platelets were isolated from blood by differential centrifuging. The leukocyte suspension was diluted by an absolute medium (RPMI 1640, embryonic calf serum, L-glutamine, antibiotics) up to 5 x 10(6) cells in 0.5 ml; while the blood platelet suspension was diluted to 05 x 10(8) in 0.5 ml, and they were cultivated for 15 at 37 degrees C. The concentration of NO nitrite metabolite was determined by Griss reaction. The NO content in leukocyte supernatant of healthy persons amounted to 0.38 +/- 0.03 nmol/0.5 x 10(6) leukocytes; while in patients this figure essentially increased--up to 1.06 +/- 0.08 nmol/5 x 10(6) leukocytes, (p < 0.001). The NO content in blood-platelet supernatant amounted, in the normal condition, to 1.07 +/- 0.07 nmol/0.5 x 10(8) blood platelets; in the victims it was 1.52 +/- 0.11 nmol/L blood platelets, (p < 0.01). The relative production of NO by leukocytes was found to be, in healthy persons, 0.75 +/- 0.06 mumol/L, (p < 0.001), in patients--3.05 +/- 0.22 mumol/L, (p < 0.01). The absolute NO concentration was determined with regard for an actual content of leukocytes and blood platelets in each healthy person and in each patient with thoracic and abdominal wounds. The absolute production of NO by leukocytes was, in healthy persons, 0.47 +/- 0.05 mumol/L, in patients--2.29 +/- 0.23 mumol/L, (p < 0.001). The absolute generation of NO by blood platelets was, in norm, 7.70 +/- 0.55 mumol/L, and in patients--11.45 +/- 0.84 mumol/L, (p < 0.0011). Consequently, the absolute production of NO by blood platelets is by 16 times higher than the absolute production of NO by leukocytes in healthy people. Thus, stress enhances the NO generation by both leukocytes and blood platelets.

APACHE↗
PubMed2003

[Criteria for assessment of endogenous intoxication in burn trauma].

Registered in patients with burn trauma was the presence of endogenous intoxication (EI), which was determined by a higher value of coefficient CLP/AOS, a higher contents of medium-molecular peptides (MMP), a lower total and effective concentration of albumin (TAC and EAC) and by a reserve of the binding albumin ability. Intoxication coefficients, i.e. IC MMP/EAC and IC C/EAC showing the deposition and binding of toxic ligands, were acknowledged as the most informative EI parameters.

Adult↗
PubMed2001

[Pathogenesis of arterial hypertension in the Itsenko-Cushing syndrome].

The search and measurements of the activity of angiotensin-converting enzyme (ACE) and glucocorticoid receptors of type II (GR II) were made in the adrenals of 19 patients with Icenko-Cushing syndrome (ICS). ACE and GR II were detected in the tissues of the adrenal cortex and cortisol-producing tumors. It is suggested that glucocorticoids may induce ACE activity and in this way potentiate synthesis of angiotensin II. The effect is mediated by GR II. Activation of such tissue components of the renin-angiotensin system contributes much to the mechanism underlying arterial hypertension.

Angiotensin II↗
PubMed2001

[Adrenal ACE and type II glucocorticoid receptors in primary hyperaldosteronism].

Adrenal tissue from 6 patients with primary hyperaldosteronism has been examined for the presence of angiotensin-converting enzyme (ACE). Its activity and amount of glucocorticoid receptors of type II (GR-II) were measured. ACE and GR-II were detected in adrenal tissue. GR-II induce ACE activity in interaction with plasma hydrocortisone. The glucocorticoid-receptor mechanism is an essential element in regulation of ACE activity determining a vasopressor effect. Disclosed is one of the aspects of tissue renin-angiotensin system function in primary hyperaldosteronism.

Adrenal Cortex↗
PubMed2001

[Receptor mechanisms for realizing the effect of glucocorticoid hormones in traumatic and hemorrhagic shock].

Blood corticosterone concentrations showed a 2-fold increase in traumatic and hemorrhagic shock. Following 4 hours of injury, the rat hepatic cytasol density of glucocorticoidal receptor II and III decreased to 76 and 67% of the level of intact animals, respectively. There were changes in the physicochemical properties of glucocorticoidal receptors: an increase in Ka and a decrease in Kd of the hormone-receptor complexes. A direct relation was found of the glucocorticoid-binding capacity of receptors II to blood pressure (BP) in shock. The most marked suppression of receptors II was noted in hemorrhagic shock, which seems to be due to more profound systemic hemodynamic changes and low BP in this type of shock. There was a concurrent reduction in the density of receptors I and II up to the certain decrease in the levels of receptors II, then was an increase in receptor III binding of [3H]-corticosterone. With the low density of receptors II and with the high concentration of corticosterone, this appears to be aimed at preserving the glucocorticoid-dependent activation of the cell genetic apparatus. Dysfunctions found in the glucocorticoidal receptors are a cause of the development of relative glucocorticoid deficiency in shock.

Animals↗
PubMed2000

[Urapidil effects on oxidative stress in hypertensive crises].

Urapidil effects on oxidant stress were studied in 36 patients with hypertension stage I-III running with crises. Acute hypertensive crisis was managed by intravenous injections of urapidil (20-50 mg) for 5 min. After that for a week they received urapidil monotherapy followed by combined treatment for another week (quinapril--25 mg/day or ramipril--5-10 mg/day in combination with hypothiaside--25 mg/day; lokren--20 mg/day or atenolol--50-100 mg/day and diltiazem--180-360 mg/day) to stabilize arterial pressure finally. Oxidant stress was estimated by lipid peroxidation (LPO) and state of antioxidant system (AOS). Catabolism and anabolism were evaluated by blood levels of hydrocortisone and insulin. LPO, AOS, the blood hormones were measured before management of hypertensive crisis, immediately after it and 1, 3, 7 and 14 days after. Before the crisis treatment LPO was found high. Urapidil administration reduced levels of hydrocortisone, dienic conjugates, lipid peroxidation, oxidant stress rate (OSR). Later, LPO and OSR slowly increased. It is concluded on validity of the antioxidants use in hypertensive patients with crises.

Acute Disease↗
PubMed1998

[Rapid method of measuring angiotensin converting enzyme activity in blood].

A simple and rapid spectrophotometric procedure is developed for measuring the activity of angiotensin-converting enzyme (ACE) in human serum. Furylacryloyl-phenylalanyl-glycyl-glycine (FAPGG) possessing a high absorption capacity at 334 nm was used as the substrate. ACE hydrolyzes FAPGG and decreases the extinction. The level of extinction drop is the measure of ACE activity. Optimal parameters of the enzymatic reaction are defined, including medium pH, substrate concentration, and volumes of the sample and inhibitor of ACE activity. Adequate control permits monitoring the interference of exogenic and endogenic factors in ACE activity in the studied sample. The proposed method is available for clinical laboratories, easily reproducible, and sufficiently sensitive.

Buffers↗
PubMed1998

[Biochemical criteria for assessing the severity of the status of wounded patients with gunshot damages to the chest and abdomen].

The biochemical assessment of severity was made in 34 patients with thoracic and abdominal gunshot wounds (12 uncomplicated; 11 with purulent, and 11 non-purulent complications). The levels of hormones, biogenic amines, lipid peroxidation (LP) indices, and antioxidant system (AOS) in serum were studied in 1, 3, 7, 14 days after admission. It was documented that the integral indices: cortisol/insulin and LP/AOS ratios were the most informative biochemical criteria for the assessment of severity of the injured patients. A high informative significance of these indices in the assessment of severity of homeostatic disturbances is pathogenetically substantiated due to stress-realizing (cortisol and free-radical LP components) and stress-limiting (insulin and AOS components) factors.

Abdominal Injuries↗
PubMed1994

[Nonsteroidal antiinflammatory agents as modulators of glucocorticoid function of receptors].

The modulating effect of nonsteroidal antiinflammatory drugs (analgin, amidopyrine, sodium salicylate) on the function of types II and III glucocorticoidal receptors of cytosol in the Wistar rat liver was studied by Scatchard's and Laynuiver-Bark's analyses and dissociation rate constants for steroid-receptor complexes, by using natural and artificial glucocorticoids having a high specific activity. Analgin was not competitive in inhibiting the function of type II glucocorticoid receptors, decreased the association constant, increased the dissociation rate constant and reduced the elimination half-life of the labelled triamcinolone acetonide from the receptor. The density of type III glucocorticoidal receptors was many times increased with analgin. Amidopyrine had no noticeable effect on the function of type II glucocorticoidal receptors, however, repeatedly enhanced the density of type III glucocorticoidal receptors. Sodium salicylate was not competitive in suppressing the function of type II glucocorticoidal receptors and increased the number of sites of binding 3H-corticosterone to type III glucocorticoidal receptors. The latter fact can explain the mechanism of action of these drugs.

Aminopyrine↗
PubMed1990

[Characteristics of the postoperative period in diabetes mellitus type 1 in patients with distal splenorenal anastomosis].

Eight patients with type I diabetes mellitus have been operated on to form a distal splenorenal anastomosis (DSRA). A critical period (the 6th and the 7th days) postoperation has been observed when severe metabolic acidosis develops; to prevent its development, transfusions of 4% sodium bicarbonate solution (1.5-2.01) have been administered before the critical period for 24 hrs, with the metabolic condition monitored by biochemical analyses. Studies of metabolism in these patients after surgery have revealed a complete normalization of the acid-base balance and of potassium level, as well as a reduction of the blood glucose concentration. The doses of exogenic insulin have been reduced by 30%, this being associated with a tendency to an increase of the levels of endogenic insulin, C-peptide and glucagon of the blood. This helps a better stabilization of the diabetic process after the formation of a DSRA.

Adult↗
PubMed1989

[Laparoscopic drainage of the gallbladder in acute cholecystitis].

Seventy-three patients with acute cholecystitis were subjected to laparoscopic drainage of the gallbladder during treatment. The endoscopic operations produced a good clinical effect in all of them. The results of the study showed that the changes of the function of the liver and the disorders of homeostasis processes occurring in acute cholecystitis regress quite rapidly under the effect of laparoscopic drainage of the gallbladder. Restoration of hepatic function and normalization of the main homeostasis parameters were used for determining the optimal terms for conducting radical operation.

Acute Disease↗
PubMed1989

[Glucocorticoid receptors as targets for pharmacologic action].

Experimental data demonstrate the influence of certain drugs on the interaction of Type II and III glucocorticoid receptors of the liver cytosol and labelled natural and synthetic glucocorticoids. Preparations of the phenothiazine (aminazine, tizercine) and pyrazolone (amidopyrine, analginum) series and non-steroid anti-inflammatory drugs (acetylsalicylic acid, sodium salicylate) exert a significant effect on the glucocorticoid-receptor interplay. Certain drugs (tizercine, analginum) have an anti-stress effect by lowering the level of Type II glucocorticoid receptors of liver cytosol and corticosterone concentration in the blood plasma of rats. The phenothiazine and no-spa derivatives inhibit the matrix activity of the thymocyte DNA in adrenalectomized rats. Pyracetam, caffeine, adrenaline, noradrenaline, verapamil, digoxin, and streptomycin do not influence the thymocyte DNA matrix activity in the presence of triamcinolone acetonide. Based on the literature data and original research findings, the problem of glucocorticoid receptors employment as targets for medication to control the glucocorticoid effect and stress is discussed.

Analgesics↗
PubMed1989

[Effect of hyperbaric oxygenation on the corticosterone content of the blood in experimental acute respiratory distress syndrome].

The three series of experiments conducted on 139 adult wistar rats it was found, that two-hour stay of the animals in barochamber under the pressure of 3 atmospheres reduces considerably the percentage of mortality rate and decelerates the development of arterial hypoxemia in rats with an experimental model of acute respiratory distress syndrome (ARDS) reproduced by intrapleural injection of oleic acid (0.27 ml/100 g). Stalle in comparison with the control (I) series elevation of corticosterone in the animal blood II and III series (conduction of HBO correspondingly in 4 and 12 hours from the beginning of the process) is considered as the manifestation of one of the most important mechanism of organism adaptation to the development of acute hypoxia in ARDS.

Acute Disease↗