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Biomedical subjects

A N Leonov

Publications and source records attributed to A N Leonov.

At least 19 recordsLinked to original sources
PubMed2001

[Phospholipase C negatively regulates tyrosine phosphorylation of EGF receptor in A-431 cells].

It is known that EGF induces tyrosine phosphorylation and internalization of the EGF receptor in A-431 cells. U73122, an inhibitor of phospholipase C, induces tyrosine phosphorylation of the EGF receptor and its association with phospholipase C still in nonstimulated cells. In U73122 treated cells EGF exerted no effect on these processes. Receptor-mediated endocytosis was not observed in A-431 cells treated with U73122. The reorganization of actin cytoskeleton was detected in U73122 cells.

ErbB Receptors↗
PubMed1991

[Effects of hyperbaric oxygenation on activation of immunocompetent cells and lipid peroxidation under immunization by heterologous erythrocytes].

On the basis of rats' experiments under conditions of HBO a close relationship was established between the intensity of immune processes and peroxide oxidation of lipids (POL). The study enabled to show a connection between immunoreactivity stimulation in spleen cells and certain levels of POL intensity and anti-oxidation protection as well. There were assessed diverse HBO effects on intact and immune organism and hyperbaric dependence of immunodepression on POL's intensification.

Animals↗
PubMed1985

[Importance of adrenoreactive vessels in the mechanisms of the vasoconstrictor response to hyperoxia].

Experiments in 116 white rats showed that high--pressure oxygen (3 beta 3.9 kPa--50 min) increased the adrenoreactivity of vessels under stimulation of alpha--adrenoreceptors with mesaton (phenylephrine) and lost this ability after blockade with pyroxan. The vasoconstricting response (the increase of blood pressure and of general peripheral resistance of vessels) seem to stem from interaction of high--pressure oxygen with post--synaptic alpha--adrenoreceptors of vessels.

Adrenergic alpha-Agonists↗
PubMed1985

[Quantitative evaluation and prognosis of the biological effects of hyperoxia].

Experiments in 104 white mice subjected to hyperoxia at different regimens of oxygenation, carried out by means of mathematical modelling of three hyperoxic effects (bradypnea, convulsions, lethality) revealed the dependence of biological (physiological, toxic) effects of hyperoxia upon both components of the oxygenation regimen (oxygen pressure, time of exposure). The proposed concept of integral dose allows to determine pressure-exposure correlations corresponding to a given biological phenomenon and to prognosticate the effects of hyperoxia.

Animals↗
PubMed1985

[Modeling of myocardial lesions of varying degrees of manifestation].

Five variants of myocardial lesions of different degree were simulated in experiments on 8 dogs, 61 rabbits and 30 rats, namely micronecrosis, diffuse myocarditis, focal dystrophy, small- and large-focal myocardial infarction. The experimental models of heart lesions can be used for studying the pathophysiological mechanisms in cardiac pathology and evaluation of the therapeutic efficacy of new drugs in experimental pharmacology.

Animals↗
PubMed1985

[Enzyme activity and content of glycerophosphate shuttle metabolites in the cortex and medulla oblongata during hyperbaric oxygenation therapy of acute hemorrhage].

The experiments on cats have demonstrated that hyperbaric oxygenation (303.9 kPa, 60 min) in acute blood loss (24.0 +/- 0.8 ml/kg) has an essential effect on glycerophosphate shuttle mechanism: it stimulates mitochondrial glycerol-3-phosphate dehydrogenase in the sensorimotor cortex and medulla oblongata, providing glycerol-3-phosphate dehydrogenation, activates cytoplasm hydrogen delivery to mitochondrial respiratory chain, prevents glycerol-3-phosphate and NADH level increase and cytoplasm glycerol-3-phosphate dehydrogenase inhibition, limiting lactate production.

Animals↗
PubMed1983

[Bioenergetic processes in the cerebral cortex and diensephalon during hyperbaric oxygenation therapy of acute blood loss].

It has been demonstrated in experiments on 134 cats that during acute blood loss (24 +/- 0.8 ml/kg), hyperbaric oxygen therapy (3039 hPa, 60 min) stimulates cytochrome oxidase, eliminates compensatory activation of mitochondrial creatine kinase and maintains the hyperactivity of cytoplasmic creatine kinase in the diencephalon, stabilizes the elevated AMP content at the level of blood loss compensation stage, prevents the fall in pO2 and in the ATP level as well as that in the energy charge and creatine phosphate content in the sensomotor cortex and subcortex, that is typical for the decompensation stage. Besides, hyperbaric oxygen therapy also averts the development of the terminal state that supervenes in the majority of untreated animals.

Adenosine Diphosphate↗
PubMed1983

[Metabolic and ultrastructural characteristics of myocardial contraction in experimental small focal myocardial infarction].

In dogs, pituitrin increases, and isadrin reduces, the tonicity of coronary arteries. Successive administration of the two agents to rabbits causes functional and metabolic unbalance of the heart, with resultant myocardial necrotic foci in the presence of blood hypercoagulation and heart muscle contractility disordered. The disorder of cardiomyocyte stereo architectonics is an essential element of the pathophysiologic mechanism of small-focal myocardial infarction.

Adenine Nucleotides↗
PubMed1977

[Role of cerebral nitrogen metabolism in the mechanisms of the therapeutic action of oxygen under elevated pressure in hemorrhagic shock].

The hyperbaric oxygen therapy (3 ata O2, 60 min exposure) of hemorrhagic shock in cats (arterial pressure--60/50 mm Hg) prevents a sharp increase of ammonia, urea, alanin, gamma-aminobutyric acid content in the brain, typical of oxygen deficiency, and activates glutamine formation. The processes of ammonia detoxication connected with glutamate and glutamine synthesis intensification course more intensively in the sensory-motor cortex than in the limbic brain structures.

Alanine↗
PubMed1975

[Structural-metabolic characteristics of the myocardium in acute hemorrhage and hyperbaric oxygenation].

Histochemical and pathomorphological changes in the myocardium in acute loss of blood and hyperbaric oxygenation were investigated in experiments on 130 white rats. It was established that acute loss of blood brought about an activation of phosphorylase, a decrease in the content of glycogen, an inhibition of the activity of cytochrome oxidase and succinic dehydrogenase in the myocardium. Foci of dystrophy were formed in the subendocaridal zone of the two ventricles and septum. Oxygenobarotherapy contributed to normalization of the level of activity of enzymes, preservation of glycogen, reduced the extent of manifestation of dystrophic changes in myocardiocytes. Hyperbaric oxygenation of healthy animals led to changes in the enzymatic activity in the myocardium. Dystrophic changes were noted in individual myocardiocytes. The data obtained testify to a direct influence of oxygen on metabolism of the myocardial cells.

Acute Disease↗