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Biomedical subjects

V I Fedorov

Publications and source records attributed to V I Fedorov.

At least 19 recordsLinked to original sources

[The effect of the activation of the sympathetic-adrenal system on the pulmonary inactivation of catecholamines in rats].

Norepinephrine extraction was found to be decreased in the lungs of immobilised rats. Administration of epinephrine to intact rats up to the same level in the blood plasma as after stress, induced an increase in the norepinephrine extraction by the lungs. The data obtained suggest that norepinephrine inactivation due to immobilisation stress is unrelated to the plasma epinephrine level. The role of the lungs in the maintenance of increased plasma of norepinephrine by means of decreasing its metabolic inactivation, is discussed.

Adrenal Glands

[Cholinergic suppression of the angiotensin I-converting reaction].

I. v. administration of carbachol or neostigmine produced a dose-dependent decrease in the angiotensin I pressor response and in conversion of angiotensin I to angiotensin II in anesthetized rats. Physostigmine produced the same effects in combination with propranolol. Administration of cholinomimetics with atropine leads to no such effect. The activation of the cholinergic system seems to inhibit a formation of angiotensin II.

Angiotensin I

[The cholinergic modulation of the pressor reaction to angiotensin].

I.v. administration of acetylcholine or acetylcholine plus neostigmine produced a dose-dependent decrease of angiotensin pressor response to 59.2, 39.9, and 26.8% of basal level at 10(-7), 10(-6), and 10(-5) M/kg, resp., and to 76.4 and 56.7% of basal level at 10(-6) and 10(-5) M/kg of neostigmine in anesthetized rats. Atropine prevented these effects and increased the angiotensin pressor response to 142.1 and 168.9% of basal level at 10(-7) and 10(-6) M/kg, resp., in intact rats. The cholinergic system seems to attenuate angiotensin effect on arterial pressure.

Angiotensin II

[The effect of angiotensin II on the catecholamine content of the blood plasma in rats].

I. v. administration of angiotensin II (0.1, 0.3 and 1.0 microgram/kg/min for 5 min) raised the plasma norepinephrine level in the right atrium and carotid artery in a reverse dose-dependent manner. The veno-arterial difference decreased dose-dependently to 17.4, 7.2 and 0.1 per cent, resp., versus 21.8 per cent in the control group. The plasma norepinephrine level was decreased and the veno-arterial difference was similar to basal level at 1.0 microgram/kg/min dose of angiotensin II for 40 min. Angiotensin II seems to affect the lung uptake and inactivation of norepinephrine in phasic manner.

Angiotensin II

[Determination of catecholamines in blood plasma using high performance liquid chromatography on the "Millichrom" microcolumn chromatograph].

The authors suggest a microcolumn modification for determining the blood plasma catecholamines by high performance liquid chromatography with electrochemical detection using a Soviet chromatograph Millikhrom. The analysis includes catecholamine extraction on aluminum oxide, elution with perchloric acid, and chromatography in a 60 x 2 mm column packed with 5 microns of Silasorb sph C8 sorbent. The method permits the detection of noradrenaline, adrenaline, and dopamine in concentrations 25-3200 pg/ml in 0.5 ml of blood plasma.

Catecholamines

[Analysis of corticosteroids in blood plasma using a microcolumn liquid chromatography method].

A microcolumn variant of high-pressure liquid chromatography of human blood plasma corticosteroids using Milikhrom, a Soviet chromatograph, is suggested. The analysis involves hexane treatment of the plasma, chloroform extraction of corticosteroids, concentration of the extract, and chromatography in a 60 X 2 mm column packed with Silasorb sorbent, sph C18 (7.5 micros), methyl alcohol/water mixture (52:48) at a rate of 100 microliter/min and a detection wavelength 240 nm. The method permits an analysis of cortisone, hydrocortisone, corticosterone, and other corticosteroids with concentrations higher than 4 ng/ml.

Adrenal Cortex Hormones

[Structure of the pressor reaction to angiotensin].

In anesthetized rats, 1938 blood pressure (BP) responses to i.v. injections of angiotensin II were studied. 6 types and 21 subtypes of responses were distinguished: vasopressor response followed by BP normalizing (type 1; 42%) or by a transitory BP drop (type 2; 7%); BP elevation without its subsequent decrease (type 3; 3%) preliminary sharp increase of BP followed by a "classic" angiotensin pressor effect (type 4; 3%); biphasic response--a depressor response followed by a pressor one (type 5; 27%); depressor response alone (type 6; 18%). Depressor phases were increased by phentolamine and indomethacin, and were inhibited by atropine and spasmolytin. The responses to angiotensin II seem to have a vector character, cholinergic system attenuating this response.

Angiotensin II

[Effect of parasympathetic agents on renin secretion in vitro].

A study was made of the effect of the parasympathetic agents on renin secretion by rat kidney sections after blockade of alpha- and beta-adrenoreceptors by obsidan and dihydroergotamine. The substances under study were administered at the concentrations 10(-8), 10(-6) or 10(-4) M. Renin activity was determined by radioimmunoassay. n-Cholinomimetics (nicotine, cytiton) were discovered to have a marked inhibitory action on renin secretion, reducing it to almost zero at a concentration of 10(-4) M. n-Cholinolytics (spasmolytin, benzohexonium) produced a dose-dependent stimulation of renin secretion with a 10-20-fold maximal increase. m-Cholinomimetics (aceclidin, proserin) and quateron provoked a 3-5-fold increase in secretion without a dose-dependent effect, whereas galanthamine exerted a negligible effect. Pilocarpine and m-cholinolytics (platyphylline, atropine) reduced the secretion by 2 times without a dose-dependent effect. It is assumed that the renal cortex contains n-cholinoreactive systems that have a direct or mediated action on renin secretion and m-cholinoreactive systems that modulate the activity of the former systems.

Animals

[Dynamics of renin production by the juxtaglomerular and mesangial cells of individual rat kidney glomeruli following adrenalectomy].

Adrenal incompetence developed in rats 6 weeks after adrenalectomy without any salt and hormonal compensation. In individual fragments of the isolated glomeruli containing juxtaglomerular cells (JGC) renin activity increased 1.2 times on the average, and there was revealed renin-like activity (RLA) in the fragments containing mesangial cells (MC). Signs of intensified renin secretion (expressed in reduction of granule count, marked development of granular endoplasmic reticulum, Golgi complex and microtubules) were noted in the JGC. In MC such organoids were well developed, but no granules were revealed. The following occurred in 8 to 12 weeks with the restoration of the 11-OCS and sodium level in the plasma: renin JGC activity became normal, RLA activity in MC disappeared, and the initial ultrastructure of both of these cells was restored. The reserve role of MC as the source of renin-like substances was confirmed.

Adrenal Glands

[Methods of determining renin activity in individual renal glomeruli and their fragments].

The author suggests a modification of the method for determination of renin activity in a single glomerulus and its fragments, based on the use of cold EDTA-treated plasma of nephrectomized animals as renin substrate source, instead of a complicated method of substrate obtaining from plasma. The renin bioassay method was somewhat simplified. All the procedures were conducted with the use of home-produced equipment. The principle of this modification can be used for clinical purposes.

Animals

[Reserve production of renin by glomerular mesangial cells following experimental decrease in renal circulation].

The aorta was partially constricted between the origins of the two renal arteries in rats. The renin activity was studied separately in the capillary parts of the isolated glomeruli and in their arterioles. The renin activity was found in the capillary parts of the glomeruli 3 to 4 weeks after the constriction. The rough and smooth endoplasmic reticulum and the Golgi complex of the mesangial cells were activated at this period. The authors consider these results as a confirmation of the hypothesis on the reserve renin production by mesangial cells under prolonged decrease of renal circulation.

Animals

[Effect of acute blood loss on catecholamine balance in the pulmonary circulation in anesthetized rats].

The contribution of pulmonary inactivation of catecholamines (CA) in the formation of their level in circulating blood during the development of a posthemorrhagic reaction was studied. Pulmonary CA inactivation was evaluated according to the arteriovenous difference (right ventricle and carotid artery) in epinephrine (E) and norepinephrine (NE) whose concentration was determined by the method of highly-effective liquid chromatography with electrochemical detection. Reciprocal phase changes in the dynamics of the arteriovenous difference in NE and E and levels of the corresponding CA in arterial blood plasma were discovered during the development of the posthemorrhagic reaction. Pulmonary inactivation of CA increased by the 2nd minute, then dropped below the initial level with subsequent restoration. The NE level in the arterial blood plasma was marked by a strictly contrary dynamics, while the concentration of E reached maximum when inactivation of E in the lungs was minimal (5th minute). The mechanisms and physiological significance of the discovered phenomenon are discussed.

Acute Disease