Publications by authors named "Arefolov V"

In experiments on rats with different resistance to oxygen deficiency (high-resistant--HR, and low-resistant LR animals) the myocardium ultrastructure of nonadapted and adapted rats was studied. It was shown that there were more glycogen granules and lipid drops initially in cardiomyocytes of nonadapted HR animals in comparison with LR ones. After a long-term adaptation to hypoxia the hypertrophia and hyperplasia of mitochondria, the nucleus and endoplasmatic reticulum hypertrophy were observed.

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The morphofunctional state of different links of the sympathoadrenal system under the action of neuroleptics haloperidol and sulpiride was studied on the model of immobilization stress in rats. The drugs were shown to possess the effect of the pharmacological correction of hormone content in the adrenals and the level of the neuromediator activity of the adrenergic nerves at different stages of immobilization stress. The data obtained indicate the anti-stress action of the studied neuroleptics.

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The antistress affect of the substance P1-4 N-terminal fragment (ARG-Pro-Lys-Pro, 100 mkg/kg, i.p.) has been studied on the model of immobilization stress in rats.

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The mediator activity of the peripheral catecholaminergic systems (the adrenergic nerves of dura mater and the concentrations of noradrenaline and adrenaline in the adrenals of rats) during dynamic and immobilization stress was investigated with the help of fluorescent microscopy and spectrofluorometry. Neuropeptides--dalargin and another enkephalin analog--were injected intraperitoneally, 150 mg/kg. A visible antistress action of these neuropeptides has been demonstrated, it was more marked after treatment with dalargin.

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Two structurally related tetrapeptides, the N-terminal tetrapeptide of substance P SP(1-4) and tuftsin, exerted some similarities in modifying immune reactions and normalizing stress-induced disorders in the catecholamine system of adrenals. This paper presents results about the effects of tuftsin and SP(1-4) on the cholinergic-adrenergic interaction in rat adrenal gland slices. Both, tuftsin and SP(1-4) inhibited the nicotine-evoked [3H]noradrenaline outflow (postsynaptic effect), but the effect of SP(1-4) was more pronounced.

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The ultrastructural organization of secretory granules, containing adrenaline (A) or noradrenaline (NA) was studied in chromaffin cells of the rat adrenal gland after 3-, 24- and 48-hour immobilization stress. Using cytochemical electron microscopic Tranzer's method and the method of morphometry, the number of normal dense cores, "empty" and "semiempty" vesicles was calculated. It was shown that the total content of vesicles and the ratio of investigated types of both adrenaline- and noradrenaline-accumulating granules were markedly changed during stress.

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Independent peptide fragments of pro-opiomelanocortin molecule, beta-endorphin and ACTH, have been detected immunohistochemically in the adrenal glands of rats and mice. Immunoreactive beta-endorphin and ACTH have been revealed in the adrenal medulla and reticular zone of the adrenal cortex. beta-endorphin and ACTH distribution patterns in adrenal sections were identical, which is indicative of the linked synthesis of these peptides in the adrenal gland.

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Fluorescent microscopy and spectrofluorometry of biogenic amines were employed to study the peripheral catecholaminergic systems in immobilized rats which received sodium hydroxybutyrate. The content of catecholamines was measured in the adrenergic nerves of dura mater, vas deferens and chromaffin tissue of the adrenals. It was established that sodium hydroxybutyrate in a dose of 40 mg/kg intraperitoneally promoted returning to normal of the adrenergic mediator activity during alarm and resistance stages.

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Radioimmunoassay was used to study variation in the content of opioid peptides (leu- and met-enkephalins) in rat adrenal glands at different stages of immobilization stress. The data obtained were correlated to the content of catecholamines (CA). It was discovered that during stress, the content of peptides noticeably increased, being independent of the main pool of CA in adrenal tissue.

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Fluorescent microscopy and spectrofluorometry of biogenic amines were used to study adrenergic innervation of the dura mater, vas deferens and medullary substance of the adrenals in immobilized rats treated with phenazepam. It was established that phenazepam (1 mg/kg, i. p.

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The effects of phenazepam and sodium hydroxybutyrate on the somatic manifestations, ultrastructure of the cortex and lipid content of the adrenals in rats exposed to immobilization were examined. Both the drugs had the stress-protective effect, decreasing the stress manifestations at alarm and resistance stages.

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Fluorescent microscopy combined with an assay of the intensity of nerve structure fluorescence was used to study adrenergic innervation of the rat mesentery and dura mater under immobilization stress. The adrenergic nerves were found to undergo morphofunctional changes over time. These changes were marked by a dramatic fall of noradrenaline fluorescence within the first immobilization hours, followed by rise at the 4th-6th hour of experiment.

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The influence of chronic stress on the ultrastructure of the myocardium and hypothalamus was studied in experiments on male rats with different levels of emotional-behavioral reactivity. "Emotional" rats manifested a pronounced increase in glycogen granules in myocytes and intercellular space, appearance of the areas of overcontraction of myofibrils, conglomerates of aggregated platelets in myocardial capillaries, and red cell egress from myocardial and hypothalamic capillaries. Alterations in the ultrastructure of the myocardium and hypothalamus in "nonemotional" rats were less marked and consisted in the appearance of the areas of overcontraction of myofibrils, enlargement of sarcoplasmic reticulum caverns, and in an increase in the lipid content in cardiomyocytes.

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Ultrastructural organization of chromaffin cells of rat adrenal glands was studied in different stress models (48 h of running in the wheel, 48 h of immobilization, and sleep deprivation during 7 days). It was shown by ultrastructural morphometry that chromaffin cells experienced fine structural modifications (a decrease in the number of adrenaline- and noradrenaline-containing granules, swelling of mitochondria and endoplasmic reticulum). The degree of such modifications depended on a stress situation, being more pronounced during physical stress.

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The effect of new tetracyclic antidepressants pyrazidol and inkazan on adrenergic neurotransmission in the isolated rat vas deferens was studied by examining vas deferens contractions in response to the transmural electric stimulation of the postganglionic sympathetic nerves and addition of noradrenaline (NA) or BaCl2. Pyrazidol and inkazan were found to be capable to increase vas deferens contractions in response to transmural electric stimulation or addition of NA. When given in high concentrations, these antidepressants inhibit the adrenergic neurotransmission since inkazan possesses low sympatholytic activity and pyrazidol exhibits certain alpha-adrenolytic effect.

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Effect of the GABA-ergic drugs, sodium hydroxybutyrate, n-dipropylacetate (n-DPA) and piracetam, has been studied on the level of homovanillic acid (HVA) and activity of GABA-transaminase in the striate body of the rat brain. It has been established that piracetam in doses of 500 and 400 mg/kg, n-DPA in a dose of 200 mg/kg and sodium hydroxybutyrate in a dose of 500 mg/kg do not affect the HVA level or activity of GABA-transaminase. The data obtained are likely to support a suggestion about a possible relationship between the GABA-ergic and dopaminergic mediator system.

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It has been shown that carbidine increases the level of homovanillic acid (HVA) in the corpus striatum of the rat brain. The changes in HVA level allowed forming a judgement on dopamine turnover. By the intensity of this effect, carbidine proved inferior to typical neuroleptics--triphtazine and ftorfenazin.

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The ultrastructure of myocytes of the rat myocardium and skeletal muscles was studied in the control during physical exercise and under conditions of two-week sodium hydroxybutyrate pretreatment. It was shown that single maximum physical exercise caused significant changes in the fine structure of cardiomyocytes and somewhat less changes in a pronounced intermyofibrillar edema, the swelling of mitochondria and an acute fall of the glycogen level. A two-week sodium hydroxybutyrate pretreatment prevented the changes in the myocytes.

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It was established that single administration to rats of 200 mg/kg of lithium hydroxybutyrate releases noradrenalin from the terminals of hypothalamus adrenergic fibers and increases output of polypeptides in the neurons of supraoptic and paraventricular nuclei of the hypothalamus. After repeated administration of the drug (200 mg/kg) once a day over 6 days) the nuclei showed depressed output of polypeptides.

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Spectrofluorometric determination of the noradrenaline content in the non-purified fraction of the rat's brain stem synaptosomes and radioisotope method resulted in finding that carbidine is capable to release noradrenaline from the nerve endings. Azabutyron, droperidol and fluphenazine had no noticeable effect on this process. The release of noradrenaline with carbidine depends upon the presence of Ca2+ ions in the medium.

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Nonachlazine (2 micrometer) blocked significantly the uptake 1 of endogenic noradrenaline in the myocardial tissues and in adrenergic neurons of vas deferens. The uptake II, as well as the intensity and dynamics of the noradrenaline release were not affected by nonachlazine. These processes resulted in an increase of free noradrenaline concentrations in the synaptic space.

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By employing fluorescent histochemistry and spectrofluorimetry the influence of an original psychotropic substance -- carbidine on the level, localization and accumulation of the adrenergic mediator in Vas deferens, dura mater and the kidney capsule was studied "in vivo" and "in vitro". Carbidine was shown to capable of liberating the adrenergic mediator from the sympathetic nerve fibres of the peripheral tissues without affecting the capture and accumulation of exogenous norepinephrine by adrenergic nerve fibres.

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