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Biomedical subjects

A A Rodionov

Publications and source records attributed to A A Rodionov.

At least 19 recordsLinked to original sources
PubMed1993

[The compensatory-adaptive mechanisms in nitrite-induced hypoxia in rats].

Concentration of blood proteins, alpha-amino nitrogen, cGMP and endothelin-1,2 was studied in rat's blood at nitric hypoxia. The injection of NaNO2 (5 mg/100 g body weight) was followed by decrease in total protein, albumin and hemoglobin content and by sharp increase in methemoglobin and Hb-NO complexes concentration in rat's blood. Simultaneously, the elevation of free amino acids and peptides with m.w. 2500 D in blood was discovered. One of these peptides was the endothelin-1,2, whose concentration increased twice in plasma at nitric hypoxia. The increase in endothelin and cGMP concentrations is mostly linked with activation of compensative mechanisms, arising as a response to high concentrations of nitro compounds and NO in rats.

Adaptation, Physiological↗
PubMed1990

[Correlations in the development of the spinal cord, dura mater and spinal canal in humans].

The spinal cord axial structures (AS) (its dura mater and vertebral canal) demonstrate the greatest growth rate during the intrauterine period and on the 18th month. After birth for the dura mater this age is 3 years, and for the spinal cord and the vertebral canal--7 years of age. The pubertal jump in growth of these formations is noted during the adolescent age (17-21 years). During the first two decades AS demonstrate asymptotic type of growth. In AS development the following periods in common have been revealed: a) intensive growth in children up to 7 years of age; b) growth stabilization (from 8 up to 16 years of age); c) period of a relative morphological stability (22-35 years); d) period of unstable compensatory-adaptive rearrangements (36-60 years); e) period of involutive changes (61-90 years).

Adult↗
PubMed1989

[Structure and dynamics of the size of the epidural space in human fetuses and newborn infants].

Basing on our definition of the ES as a complex of peridural anatomical formations and taking into account certain peculiarities of their topographic distribution, 4 areas (anterior, posterior and two lateral) are defined. The posterior area of the ES by its sizes predominates over all the others. The ES value is determined by differences in rates of size increment of the vertebral canal and in rates of size increment of the spinal cord dura mater (SCDM). Position of the SCDM sac concerning the central axis of the canal predetermines++ the size of the ES four areas. The dimensions of the ES areas are not similar at various levels of the spinal column. For example, the dimensions of the ES posterior area in newborns are the greatest in the cervical part at CVII, in the thoracic--at ThIV-VII, in the lumbar--at LI-III, and the dimensions of the ES anterior area--at CVII, ThI-IV, LIV-V and Sr. The lateral ES areas are the widest at CI, ThIII, LV and SI. The greatest increase in the rate of increment of linear sizes and area is observed for the spinal canal and spinal cord in 5-, 8- and 9-month-old fetuses and for SCDM--in 5- and 8-month-old fetuses and for ES--in 6-, 8- and 9-month-old fetuses. The topographic peculiarities in the ES structure revealed and rearrangement of its dimensions in the fetuses and newborns can be useful in interpretation of problems on functional formation of the vertebral column, spinal cord and its tunics, and be of applied aspect at various manipulations performed in these formations in premature infants and in newborns.

Cervical Vertebrae↗
PubMed1984

[A method of rapid extraction of the whole vertebral column during autopsy].

The method is a follows: the cervical part of the vertebral column is mobilized from the inner cranial base with the preservation of the occipito-atlantic joint and with subsequent cranio-caudal extraction. This method does not disturb the epidural space and allows the extraction of the vertebral column without any assistance within 30 minutes.

Autopsy↗
PubMedDate not supplied

[The antidystrophic effect of the action of beta-adrenoblockaders in local damage to the nervous system].

It has been established that the lesion of the sciatic nerve, accompanied by a disturbance of normal neurotrophic provision of a kidney as a result of coming to the organ of the perverted nervous stimuli (by the neuro-conductive path through sympathetic nerves and by participation of the hypothalamus--hypophysis--peripheral glands system), leads to disturbance of functioning of mineral-corticoid receptors of kidneys. It has been also established that simultaneous pharmacological blockade of neuro-conductive and humoral pathways of transmission to the kidney of pathological stimuli from the central stump of the cut sciatic nerve prevents the development of trophic organ disturbances, tested by the state of the kidney mineral-corticoid receptor apparatus, while pharmacological stimulation of sympathetic nervous system leads to the greater disturbance of aldosterone reception by the cells of kidney channels. A valid conclusion can be made that propranolol is a substance, which may weaken possible non-adequate reactions of peripheral tissues to the action of physiologically active substances during the development of the consequences of the lesion of the nervous system and thus to prevent the development of neurogenic dystrophies.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[The mineralocorticoid receptor apparatus of the kidneys in rats with reflex dystrophy of the organ against a background of simultaneous denervation or blockade of the body beta-adrenoreceptors by propranolol].

Interaction of labeled aldosterone with rat kidney mineral corticoid cytoplasm receptors and duct cell nuclei at different dysfunctions of nervous-trophic organ supply. Dysfunction of vagus innervation leads to breakage of cytoplasm receptor apparatus and duct cell nuclei that performs aldosterone reception. Organ denervation and introduction of beta-adrenoblocking agent prevents development of kidney neurogenous dystrophy.

Aldosterone↗
PubMedDate not supplied

[Sodium reabsorption and the aldosterone receptors in the cells of the kidney tubules in a dynamic disorder of the trophic function of the nervous system].

The results are presented of investigations on determining the functional state of mineralocorticoid receptor apparatus in rat kidney at diverse stages of the reflex renal dystrophy per se and that against the background of renal denervation along with propranolol injections produced at different terms following the disturbance of nervous system trophic function. It was shown that simultaneous blockade of neuroconductory and humoral pathways of pathological stimulus transmission from central end of cut ischiatic nerve to the kidney prevents the development of trophic disturbances in the organ as tested by the state of mineralocorticoid receptors, to a more extent than the blockade of neuroconductory pathway only. The activity of molecular structures which determine the mineralocorticoid reception in cells of renal tubules seems to be controlled both by central neuroconductory and humoral mechanisms.

Absorption↗
PubMedDate not supplied

[Neurogenic dystrophy of the rat kidney and interaction of aldosterone with cytoplasmic and nuclear receptors of kidney tubules].

Dystrophy of rat kidney caused by denervation did not affect the binding of 3H-aldosterone with specific receptors of cytoplasm and nuclei in the small tubular cells. But under conditions of reflectory dystrophy the rates of 3H-aldosterone binding with cytoplasm receptors as well as the hormone transmission from cytoplasmic to nuclear receptors were decreased. The impairments observed in molecular mechanisms of the aldosterone consumption in kidney tubular cells may be responsible for alterations in the tissue sensitivity to the hormone, which was expressed primarily as deterioration of the Na+ reabsorption in the neurodystrophic injury.

Aldosterone↗
PubMedDate not supplied

[Reception of aldosterone by the rat kidney in its compensatory hypertrophy].

A study was made of the effect of the compensatory hypertrophy of the rat kidney (on the 30th day) on the interaction of 3H-aldosterone with the receptors of the kidney cell tubules. It has been shown that the compensatory hypertrophy of the kidney is accompanied by an increased intensity of 3H-aldosterone binding with the receptors of the nephron cell cytoplasm and a decrease of the transfer of the hormonoreceptor cytoplasm and 3 receptor complex to the nucleus. These changes in the mechanism of aldosterone reception by the hypertrophic kidney can be accompanied by disturbed sensitivity of the organ to this mineralocorticoid.

Adaptation, Physiological↗