Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova最新文献

Neural activity in two symmetrical areas of the prefrontal cortex left and right hemispheres of the rat brain (55 and 47 neurons, respectively) were recorded during the execution of behavioral tasks in the two-ring maze. Experiments were carried out in two different conditions - task with the key, when only appropriate side to signal was reinforced, and without a key, when any choice was reinforced. Differential neural activity was estimated - the level of difference in firing on the right and left choice. When the animal did not guided by external keys (two behavioral situations: trails in a behavior block without any keys or error trails in behavior block with key presentation) there was observed prevalence of differential activity in the left hemisphere. The prevalence in the right hemisphere was observed in the correct trials in behavior block with key presentation. Apparently this is evidence of the dynamics in the hemispheric balance, depending on the external and internal conditions and the special role of the right hemisphere in the mechanisms of learning and inclusion of external determinants of the adaptive behavior response.

Lactoferrin - multifunctional glycoprotein of the transferrin family with a molecular mass of about 80 kDa. We studied the effect of human lactoferrin on stress-induced changes in the level of corticosterone and adrenocorticotropic hormone (ACTH) and redistribution of leukocytes in the blood of rats. The used model of stress - swimming in cold water (1-4 °C) for 2 minutes. Corticosterone and ACTH levels in the plasma were determined by enzyme immunoassay. It has been established that preventive intraperitoneal administration of lactoferrin has reduced stress-induced increase in the concentration of corticosterone in 30 minutes after the stress and has normalized stress-inducing changes in the number of neutrophils in the blood after 30 minutes and 3 hours after exposure of stress, but has not affected the level of ACTH. The results of this study suggest that lactoferrin can act as an adaptogen during experimental stress.

Effect of mast cell degranulation blockade on the inflammatory response and character of the lung tissue structure-functional changes were evaluated in the chronic obstructive pulmonary disease model produced in rats by 60-day intermittent exposure to nitrogen dioxide. The membrane stabilizer sodium cromoglicate was used to blockade of mast cell degranulation. Lung tissue sections were stained with toluidine blue to identify mast cells. Bronchoalveolar lavage fluid (BALF) cytogram was determined. The levels of mast cell tryptase and chymase, proinflammatory cytokine TNF-α, surfactant protein B were measured in BALF. Suppression of mast cell degranulation prevented the release of proteases in the bronchoalveolar space and reduced activity of the inflammatory process. The influx of inflammatory cells and TNF-α concentration decreased. There was no interstitial inflammatory infiltration. Bronchoalveolar epithelium structure was recovered that is the basis of its functional usefulness. The results confirm the active involvement of mast cells in the development of the inflammatory process in obstructive pulmonary diseases and allow us to consider them as a possible therapeutic target.

In acute experiments on the anesthetized rabbits the pulmonary hemodynamics changes following pulmonary thromboembolism were studied in animals with intact circulation and isolated lungs perfusion in the control series and after the blockade of the alpha-adrenoceptors. Following pulmonary embolism in animals with intact circulation in the control group and after the blockade of alpha-adrenoceptors the pulmonary artery pressure and pulmonary vascular resistance increased, but the pulmonary artery flow decreased to the same extent. However, in control animals, the cardiac output decreased more, than the pulmonary flow; the superior vena cava flow was decreased less, than inferior vena cava flow. After the blockade of the alpha-adrenoceptors there were no any imbalance between the decreasing of the cardiac output and pulmonary flow as well as between the decreasing of superior and inferior venae cavae flows. In animals with perfused lungs after the blockade of the alpha-adrenoceptors the pulmonary artery pressure following pulmonary embolism increased to the same level as in animals with intact circulation, however, in the first case the pulmonary vascular resistance increased four times less than in the last one. Thus, we concluded, that following pulmonary thromboembolism the activation of the alpha adrenergic mechanisms could not only promote to increase the resistance of the pulmonary vessels, but these mechanisms are also involved in the changes of the capacitive function of the pulmonary vessels.

Currently there is no single answer on the question of the participation of nitric oxide and NO-synthase (NOS) in the cardioprotection in the early phase of ischemic preconditioning (IP). In the present review the results of experimental studies indicate the involvement of NOS in the protective effect of IP and the literature data refuting this assumption. In addition, it was presented data on the increase of nitrates and nitrites (the stable metabolite of NO) in myocardial tissue after the IP, an increase in the expression of genes encoding NOS immediately after the IP, the data on the elimination of the protective effect of IP of NOS blockers and of imitation of IP affects IP by nitric oxide donors. It was exhibited a brief analysis of some of the studied mechanisms involving NO and NOS in cardioprotection at IP.

It was investigated the role of δ-, μ- и κ-opioid receptors (ORs) in the development of cytoprotective effect of chronic normobaric hypoxia (CNH) using anoxia/reoxygenation of isolated cardiomyocytes. Adaptation to CNH was achieved by the maintenance of rats for 21 days at atmosphere containing 12% O2. Anoxia/reoxygenation of isolated cardiomyocytes of intact rats evoked a death of 23% cells and enhancement of lactate dehydrogenase (LDH) release from cells. Anoxia/reoxygenation of isolated cardiomyocytes of adapting rats induced a death of only 2.5% cells and LDH release decreased by 25%. Preliminary incubation of cells with the OR blocker naloxone (300 nM) or the δ-OR antagonist TIPP(ψ) (30 nM) or the selective δ2-OR antagonist naltriben (1 nM) or the μ-OR antagonist CTAP (100 nM) 25 min prior to anoxia abolished adaptive enhancement of cell survival and a decrease in LDH release. The blocking of δ1-OR by BNTX (1 nM) or κ-OR by nor-binaltorphimine (3 nM) not affected on the cytoprotection at CNH. Consequently, cardiac cell δ2- and μ-opioid receptors are involved in the cytoprotective effect of chronic normobaric hypoxia.

Receptors of the T1R family are molecular sensors for sweet taste stimuli. They are expressed not only in the oral cavity, but in most of endocrine cells controlling homeostasis of glucose as well as in adipocytes. Earlier, we have demonstrated that deletion of the Taslr3 gene, which encodes the T1R3 protein, reduces glucose tolerance, elevates insulin resistance and cause a decrease of blood glucose level after food deprivation. The goal of the study was to elucidate an involvement of T1R3 in control of endogenous glucose synthesis and lipid metabolism. Experiments were performed with an inbred mouse strain C57BL/6ByJ and the Taslr3-gene knockout strain C57BL/6J-Tas1r3tm1Rfm maintained at the normocaloric diet. It was shown in vivo that the presence of intact T1R3 stimulates gluconeogenesis and lipid utilization during starvation and likely promotes glycogen synthesis. Additionally, T1R3 potentiates utilization of triglycerides and glycerol (in fed state) and restricts secretion of glucagon during fasting but does not affect insulin output. Thus, T1R3-mediated visceral reception of metabolites is involved in control of carbohydrate and lipid metabolism.

Tissue relative "hyperoxia" during reperfusion can cause oxidative stress due to oxygen participation in free radical processes. The influence of the hydrogen sulfide on the blood oxygen was investigated during hepatic ischemia(30 min, m.Pringle) and reperfusion(120 min) in rats. The parameters of blood oxygen (р50, Hb, MetHb, HbCO, pCO2,pO2, pH, TCO2, ABE, SBC), summary nitrite/nitrate level, plasma hydrogen sulfide and transaminases (ALT, AST) as a marker of liver damage were estimated. It's detected, that a single injection of sodium hydrosulfide (14 μmol/kg, 5 min before reperfusion) improves blood oxygen parameters (p50, pH, TCO2, ABE, SBC), plasma hydrogen sulfide and decreases transaminase levels during hepatic ischemia-reperfusion in rats. It was no changes in the MetHb or HbCO concentrations after sodium hydrosulfide infusion. The protective effect of hydrogen sulfide can be bind with increased hemoglobin oxygen affinity in the blood during reperfusion.

The present study is designed to establish how lexical frequency of Russian words influences the acoustic mismatch negativity (MMN) latency and amplitude. The event related potentials (ERP) were recorded according to the multi-deviant passive odd-ball paradigm by using Russian words with different lexical frequencies and pseudowords. We found that the high-frequency words presentation led to a significantly more pronounced MMN response relative to the low-frequency one. The high-frequency words also evoked an earlier response, indicating more rapid access to a frequently used lexical entry. We suggest that a more pronounced amplitude and an earlier latency of acoustic MMN of high-frequency versus low-frequency items is a result of the word memory traces activation as more strongly connected assemblies of neurons. The MMN amplitude and latency for words were partly matched with the MMN for pseudowords (the analog of high-frequency word evoked the most pronounced response and the analog of low-frequency word evoked the weakest response), but the MMN amplitude and latency for pseudowords were significantly more pronounced and longer. We interpret this as evidence that processing of meaningless or unknown items is longer and their discrimination is more late and inaccurate than the discrimination of meaningful and frequently activated language elements.