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Biomedical subjects

E I Chazov

Publications and source records attributed to E I Chazov.

At least 19 recordsLinked to original sources
PubMed2006

Effects of chronic neuroticization on the monoaminergic systems of different structures in the brains of rats with different typological characteristics.

The levels of monoamines and their metabolites were studied by HPLC with electrochemical detection in homogenates of hypothalamus, hippocampus, prefrontal cortex, and amygdala in intact and neuroticized Wistar rats with different types of behavior in the open field and forced swimming tests. Intact rats with intermediate levels of activity and depressivity had higher serotonin concentrations in the hypothalamus and lower noradrenaline and hydroxyindoleacetic acid levels in the hippocampus than rats characterized by low activity and high depressivity. In neuroticization, the levels of study monoamines and their metabolites decreased in all the brain structures investigated with the exceptions of an increase in the dopamine concentration in the hippocampus and the dihydroxyphenylacetic acid concentration in the prefrontal cortex. The effect of neuroticization on the neurotransmitter systems in all study structures except the hypothalamus depended on the typological characteristics of the rats. This was most marked in rats with the extreme types of behavior--active and passive--in which changes in monoamine and metabolite contents were seen in all brain structures studied. Rats of the intermediate type showed no changes in any of the substances studied in the hippocampus.

Animals↗
PubMed2006

[Depression in cardiological practice: pilot results from a multicenter clinico-epidemiological trial in hypertensive patients with ischemic heart disease (koordinata)].

AIM: To study effects of depression on the course and prognosis of arterial hypertension (AH) and coronary heart disease (CHD), potentialities of the combined treatment in a prospective multicenter trial. MATERIAL AND METHODS: A total of 376 patients with AH and/or CHD having depression (10 scores and higher by HADS scale) were assigned to two groups: 189 (50.3%) patients received somatotropic therapy+coaxil (the study group), 187 (49.7%) patients received somatotropic therapy alone (the comparison group). Coaxil was given for 6 weeks in a dose of 37.5 mg/day, to patients over 70 years--25 mg/day. The effects were assessed by changes in HADS, CGI scale, blood pressure, heart rate; by tolerance and side effects (objective effects); complaints, well- being, stress, tolerance (subjective effects). RESULTS: The addition of coaxil to somatotropic therapy of patients with AH and/or CHD associated with depression led to improvement of the psychological status (a 36% decrease by HADS depression scale from 13.1 +/- 2.75 to 8.43 +/- 3.64, -delta4.76, p < 0.0001; by HADS anxiety scale--by 35.6% from 12.08 +/- 3.90 to 7.78 +/- 3.63, -delta4.31, p < 0.0001; by response to psychoemotional stress--by 23% from 6.65 +/- 1.94 to 4.77 +/- 1.85, -delta1.88, p < 0.05). Control patients also showed a positive trend in the above indices (a decrease in the above indices from 13.15 +/- 2.65 to 11.79 +/- 3.31, from 11.50 +/- 3.66 to 10.12 +/- 3.95, from 6.63 +/- 1.99 to 6.03 +/- 2.07, p < 0.05, respectively) but positive changes were much weaker than in the coaxil group (p < 0.001). To the end of the treatment, patients of the study group had less number of complaints, more patients achieved the target level of arterial pressure under 140/90 mm Hz (43.9 versus 29.9% in the control group; p < 0.005). CONCLUSION: Standard somatotropic treatment of AH patients with CHD and depression is not sufficiently effective. Combination of such treatment with antidepressive therapy (coaxil) significantly improves psychological status, and efficacy of therapy of basic cardiological diseases.

Aged↗
PubMed2006

[Platelet activation and inflammation markers in patients with coronary heart disease and depression].

AIM: To study morphological features and functional activity of platelets, their relations with the level of inflammation markers in coronary heart disease (CHD) patients with depression. MATERIAL AND METHODS: The study group consisted of 33 CHD patients with stable effort angina (NY-HA FC I-III), 14 had depression, 19 were free of depression. Sixteen healthy volunteers comprised the control group. Platelet aggregation was registered by a mean size of aggregates and turbidometrically. Platelets shape, leukocytic-thrombocytic and erythrocytic-thrombocytic aggregates (LTA, ETA) in the whole blood were studied electron-microscopically. The levels of IL-2, IL-6, TNF-alpha, sVCAM, hsCRP were measured in the blood, serotonin--in platelets. RESULTS: Spontaneous aggregation enhanced in 52.6% CHD patients (p < 0.05). The blood contained reticular platelets, high number of prothrombocytes (p < 0.05), mean volume of thrombocytes was greater (p < 0.05). This reflected changes in megakaryocytopoiesis. Some of the patients had LTA and ETA. Out of inflammation markers, only IL-6 and sVCAM were elevated (p < 0.01), hsCRP concentration rose, but not above normal range. Serotonin in platelets was the same in the patients and controls. Depression aggravated the disorders and elevated other indices. Spontaneous aggregation was high in 71.4% of depressive CHD patients. The count of reticular platelets, prothrombocytes, mean volume platelets were also elevated. LTA and ETA were high in all the depressive patients. Elevated were also concentrations of IL-6, sVCAM, IL-2, hsCRP. Serotonin in platelets was low (p < 0.05). CONCLUSION: Depression stimulates functional activity of platelets, is a factor of risk of intravascular inflammation and contributes to development of thrombotic complications in CHD patients.

Aged↗
PubMed2005

Erythrocyte membrane fluidity and haemoglobin haemoporphyrin conformation: features revealed in patients with heart failure.

This study examined the possible involvement of abnormal erythrocyte oxygen (O(2)) transport in the pathogenesis of heart failure. Haemoglobin (Hb) haemoporphyrin conformation was assessed by Raman spectroscopy (RS) of blood samples, whereas membrane fluidity was estimated at depths of 0.6-0.8 and 2.2nm by electron-paramagnetic resonance spectroscopy of erythrocytes loaded with spin-labeled 5-doxylstearic acid and 16-doxylstearic acid, respectively. The fluidity of erythrocyte membranes from patients with heart failure was decreased in the area near the membrane surface and remained unchanged in the deeper hydrophobic membrane regions. The same differences were also detected in healthy controls subjected to chronic high-altitude hypoxia. RS demonstrated that in heart failure the total content of Hb-ligand complexes and the relative content of Hb-nitric oxide (NO) complexes with cleaved Fe(2+)-globin bond was decreased, whereas content of Hb-NO complexes with preserved Fe(2+)-globin bond was increased. We propose that this phenomenon contributes to the reduced O(2) tissue supply seen in patients with heart failure.

Journal Article↗
PubMed2005

[The role of plasmatic erythrocytic membrane in formation of hypoxia in patients with chronic cardiac failure].

AIM: To study oxygen supply to erythrocytes in patients with chronic cardiac failure as a factor provoking hypoxia. MATERIAL AND METHODS: The trial enrolled 12 men with chronic cardiac failure (CCF) of functional NYHA class II aged 37 to 74 years (group A). Group B--healthy donors (n = 10) aged 20-40 years. Conformation changes of hemoporphirine were detected with degradation spectroscopy, viscosity of plasmatic membrane--with resonance spectroscopy. Degradation spectroscopy estimated content of Hb-ligant complexes as 0.34 +/- 0.013; complexes I Hb-NO 0.73 +/- 0.11, complexes II Hb-NO 0.28 +/- 0.08 (group A). RESULTS: Electronic-paramagnetic spectroscopy has estimated: S--0.716 +/- 0.005 (group A), 0.667 +/- 0.011 (group B). In group B- 0.5 +/- 0.08; 0.41 +/- 0.22; 0.55 +/- 0.12, respectively. CONCLUSION: Patients with CHF have high microviscosity of plasmatic erythrocytic membrane near location of polar lipid groups; subnormal content of oxyhemoglobin and elevation of the number of complexes of nitric hemoglobin-oxide; altered binding of nitric oxide with hemoglobin.

Adult↗
PubMed2004

[Anticholinergic Effect of a New Antiarrhythmic Class III Drug RG-2].

In experiments on isolated rat and rabbit right atrium, a new class III antiarrhythmic drug RG-2 (0,01-1 microM) was shown to have anticholinergic action competing with 0.2-1 mM carbachol. RG-2 (0.1-1 microM) produced dose-dependent increase of APD90% in rat and rabbit atrial cells and had no effects on other action potential parameters. In presence of carbachol RG-2 produced significantly greater increase of APD90% and caused significant increase of APD50%. Thus RG-2 exerts anticholinergic action, which can take important part in RG-2 antiarrhythmic activity.

Action Potentials↗
PubMed2004

[Antiarrhythmic Efficacy of a New Class III Antiarrhythmic Drug RG-2.].

We studied effects of a new class III antiarrhythmic drug RG-2 in a canine model of vagally-mediated atrial fibrillation (AF). RG-2 was intravenously infused to anesthetized open-chest dogs in progressive doses (5, 10, 20 and 40 mg/kg, n=6) during vagally-induced AF. RG-2 significantly dose-dependently increased atrial effective refractory period (AERP) with and without vagal stimulation, but did not change conduction velocity. Five mg/kg terminated vagally-induced AF in 4 of 6 dogs but did not prevent AF reinduction. However, additional doses of drug 20 and 40 mg/kg successfully terminated AF in 100% as well as prevented AF reinduction in 50% and 72% of cases, respectively. Activation mapping (224 epicardial electrodes) showed that under drug influence there was gradual reduction of wavelet number until termination of the reentrant excitation. AF cycle length increased before AF termination from 91+/-4 to 140+/-8 ms (p<0.01). These changes correlated with drug-induced increasing of AERP. In conclusion, the ability of RG-2 to terminate and prevent reinduction of experimental AF appears to be associated with a significant prolongation of the AERP.

Animals↗
PubMed2003

[Ionic mechanisms of cardiotropic action of a new class III antiarrhythmic drug RG-2].

A perforated patch-clamp analysis of the effect of a novel class III antiarrhythmic agent RG-2, on voltage-dependent currents was made in rat ventricular myocytes. In these cells, RG-2 decreased delayed rectifier outward K(+) current, I(k), in concentration dependent manner with threshold concentration 0.1 microM/l. In contrast, the drug did not have significant effects on the transient outward and inward rectifier K(+) current. RG-2 in concentration dependent manner decreased Ca(2+) current (I(Ca,L)) with threshold concentration 1 microM/l, tenfold higher than threshold concentration for I(k). We can conclude that decreasing of I(k) may explain prolongation of cardiac repolarization induced by RG-2, and contribute to its antiarrhythmic action.

Animals↗
PubMed2003

[Electrophysiological experimental study of a novel class III antiarrhythmic drug RG-2].

The electrophysiologic effects of a new drug, RG-2 were studied on anesthetized open-chest dogs and on rabbit right atrial tissue. RG-2 was manufactured in Chemical-Pharmaceutical Institute in Moscow. Dogs (n=12) were anesthetized with sodium pentobarbital (30 mg/kg, i.v.). An ECG lead II, arterial blood pressure, His bundle electrogram, atrial and ventricular bipolar electrograms were continuously monitored, recorded and then analyzed by a computerized complex for electrophysiological study. Electrophysiological variables, ECG parameters, atrioventricular conduction (His electrogram) and blood pressure were determined after sequential i.v. administration of 1, 5, 10, 20, 40 and 80 ug/kg of RG-2. Interval between injections was 60 min. RG-2 had no significant effect on PQ, QRS, S-A, A-H and H-V intervals, but the drug caused dose-dependent increase of R-R and QT intervals. Moreover, RG-2 dose-dependently increased the atrial and ventricular effective refractory periods (AERP and VERP). Maximal increases of AERP and VERP registered at 5 min after administration of RG-2 (40 microg/kg) were 46+/-2% (p<0.001 vs control) and 23+/-6% (p<0.05 vs control), respectively. In the isolated rabbit right atrial tissue RG-2 (0.01 to 1 microM) had no effects on maximal diastolic potential, action potential amplitude and Vmax, but revealed concentration-dependent increase of action potential duration at 90% repolarization level (APD90%). The maximal effects on APD90% obtained after RG superfusion at 1 microM were 26+/-7% (p<0.001 vs control). We conclude that RG-2 has significant effects of class III antiarrhythmic drugs in vivo and in vitro.

Animals↗
PubMed2001

Monocyte integrin expression and monocyte-platelet complex formation in humans with coronary restenosis.

1. In the present study, we sought to determine whether patients with restenosis after coronary stenting possess increased monocyte reactivity, as manifested by a higher level of adhesion molecule expression and an enhanced propensity to form monocyte-platelet aggregates after activation in vitro. 2. Anti-coagulated peripheral venous blood from 24 patients, 10 with and 14 without angiographically verified restenosis, was obtained. Leucocyte antigen expression and the number of leucocyte-platelet complexes were measured by flow cytometry after activation in whole blood. 3. Surface integrin Mac-1 (CD11b/CD18) and VLA-4 (CD49d/ CD29) expression on monocytes and the relative number of monocyte-platelet complexes after in vitro activation were significantly elevated in patients with restenosis compared with patients without restenosis (fluorescence intensities of 1425 +/- 76 vs 1195 +/- 71, 87 +/- 7 vs 65 +/- 6 and 47 +/- 4 vs 29 +/- 3% for for Mac-1, VLA-4 and monocyte-platelet complexes, respectively; P < 0.05 for each parameter). 4. The results suggest that restenosis is associated with increased monocyte VLA-4 and Mac-1 integrin expression and monocyte-platelet complex formation, which can be revealed after activation in vitro.

Blood Platelets↗
PubMed2001

[Urokinase stimulates whereas tissue plasminogen activator attenuates blood vessel stenosis].

Periadventitial application of the urokinase-plasminogen activator (uPA) in pluronic gel to an injured artery stimulated the neointima and neoadventitia formation as well as cell migration and proliferation in vivo. In contrast, the tissue-type plasminogen activator (tPA) reduced the number of neointimal smooth muscle cells and neointimal area and attenuated the lumen stenosis after a balloon catheter injury of the rat carotid artery. This ability to stimulate the neointima and neoadbentitia formation was found to be quite specific for the uPA. The findings suggest that this uPA property provides a specific functional target for attenuating growth of the damage.

Angioplasty, Balloon↗