[Study of the influence of etoxidol on expression of follistatin-like protein-1 (FSTL-1) in myocardium after experimental infarction in rats]. / Issledovanie vliianiia étoksidola na ékspressiiu follistatin-podobnogo belka-1 (FSTL-1) v miokarde posle éksperimental'nogo infarkta.

In heart attack, FSTL-1 is actively secreted by cardiomyocytes, accelerates growth of heart myofibrils and stimulates of vascular endothelial growth factor expression. The aim of this work was to investigate the effect of Etoxidol on synthesis of FSTL-1 in rats after myocardial infarction. The experiments were performed on Wistar rats weighing 250-350 g with simulated myocardial infarction or intact (group 5). Animals of control groups (groups 1, 2) were treated with saline for 7 and 14 days; Ethoxidol (24 mg/kg) was injected to animals of experimental groups (group 3, 4) (the daily dose was 6.36 mg/animal) for 6 or 14 days. The injection volume was 0.2 ml. At the beginning and at the end of the study plasma concentrations of FSTL-1 were determined by the ELISA method. Myocardial FSTL-1 gene expression was determined by real-time PCR. At the end of the experiments, the hearts were also used for histochemical analysis. To determine the size of the scar formed after the modeled heart attack, we used the classic Mallory staining method. The results show that the development of experimental acute myocardial infarction is accompanied by a significant increase in FSTL-1 expression in the heart, which was detected on the 7th day and stored increased by 14 days after a heart attack. After therapy with Ethoxidol, a tendency to a decrease in the expression of FSTL-1 by the 14th day was observed; it coincided with the dynamics of the plasma protein FSTL-1 level. It can be assumed that the downregulation trend in the FSTL-1 expression is associated with a more effective repair process after a heart attack, since FSTL-1 increases precisely in response to myocardial damage and decreases when the incentives for its expression from damaged heart tissue are reduced. Indirectly, this assumption is confirmed by the detected tendency to reduce the size of post-infarction fibrosis in the treatment with Ethoxidol. The results indicate the ability of Ethoxidol to influence FSTL-1 synthesis of in rats after myocardial infarction.

The Mechanism of Action of Ethoxidol on Oxidative Stress Indices in Heart Failure and Hypotension.

The aim of the investigation was to study the effect of 2-ethyl-6-methyl-3-hydroxypyridine malate (Ethoxidol) on the concentration of oxidative stress metabolites in patients with chronic heart failure (CHF) and hypertension. MATERIALS AND METHODS: 126 patients with FC I-III CHF have been examined. In addition to their individual therapy these patients received intravenous infusions of Ethoxidol. Blood content of 2,3-diphosphoglycerate (2,3-DPG), oxygen tension (рО2), pH, concentration of total peroxides, lactate, and aldosterone were identified. 2,3-DPG levels (g/L erythrocytes) in whole blood samples were determined by an enzyme assay using the reagent kit (Rosh, Germany), values of рО2, рСО2, рН, lactate in the venous blood were measured using gas analyzer Stat Profil pHOx Ultra (Nova Biomedical, USA). Indices of oxidative stress, i.e. the concentration of plasma total peroxides, were investigated by ELISA using OxyStat kit (Biomedica, Austria). Peripheral venous blood samples were collected from all patients before and 6 days after the daily intravenous Ethoxidol infusion. RESULTS: In patients with FC I, II, III CHF, on day 7 after intravenous Ethoxidol infusion at a dose of 100 mg/day, statistically significant growth (p=0.0002) of PaO2 level by 15.7, 17.4, and 22.8%, respectively, was noted. In patients with FC I, II, III CHF in the group receiving standard therapy, statistically significant (p=0.002) reduction of 2,3-DPG level by 2.7, 2.4, and 4.0%, respectively, was registered. On day 7 after the infusion of Ethoxidol at a dose of 100 mg/day, its decrease by 5.7, 10.5, and 26.2%, respectively (p<0.0001), was also observed. CONCLUSION: The increased concentrations of active oxygen forms have been established to negatively affect various bodily functions and adversely influence the pathophysiology of numerous diseases. Application of antioxidants, including Ethoxidol presented by us in this article, may become a clue to the development of preventive measures for many serious diseases.

[Using of reamberin on patients with cerebral deficiency due to severe forms of acute poisonings].

The aim of work was to test the using of reamberin on patients with cerebral deficiency due to severe forms of acute poisonings. The investigation was made on 60 patients (38 men and 22 women), whose average age was 34.7 +/- 2.6 (for men) and 28.4 +/- 3.2 (for women). The main group was divided into two parts, which had compared age, sex and gravity of condition. The first one was given reamberin with standart therapy (I - 32 patients), the second - only standart therapy (II - 28 patients). It was revealed that using of reamberin in complex therapy of acute cerebral deficiency lead to decrease of intensity of cerebral deficiency and to increase of speed of cerebral activity rehabilitation. These changes lead to improvement of clinic tendency of cerebral deficiency, what was illustrated by decrease of comatose period from 55.0+/- 2.2 to 33.0 +/- 2.6 hours, decrease of the time of being in reanimatology department from 69.1+/- 3.6 to 53.4+/- 4.3 hours.

[Cerebral hypoxic lesions in the early phase of acute intoxications with neurotropic poisons: development, course, and ways of correction].

The paper presents the results of examination and treatment of 147 patients in the early phase of severe acute intoxications with neurotropic poisons. The use of the methods of assessing the bioelectrical activity of the brain has been found to objectively evaluate the degree of CNS suppression, to clarify the nature of the damaging action of a toxic agent, and to evaluate the efficiency of therapy. The use of cytoflavin in intensive care for cerebral hypoxic lesions has been shown to substantially decrease the degree of brain lesions.

[Mechanisms of adaptation effect of normobaric hypoxic therapy]. / Mekhanizmy adaptatsionnogo éffekta normobaricheskoi gipoksiterapii.

It was discovered that brain adaptation to long-term hypoxia operates primarily through lowering frequency of dominating spontaneous activity. EEG parameters can help in assessment of acute hypoxia and predict effectiveness of hypoxic therapy. Patients with definite response to rhythmic photostimulation in the range of alpha-activity tolerate hypoxia well. High presentation of slow waves in the pattern of the initial EEG, especially of teta-rhythm predicts formation of adaptive effect in hypoxic therapy.