Biomedical subjects
Publications and source records attributed to V I Fedorov.
The author proposes to classify gross and trace elements by the level of their investigations in physiology and biochemistry. By using the facts, he discusses whether X-ray fluorescence and spectral analyses with inductively-bound plasma may be to develop an adequate procedure that can determine the serum content of the maximum possible number of chemical elements during one analytical procedure.
We measured activity of angiotensin-converting enzyme in plasma and tissue of NISAG and normotensive WAG rats. In different organs of NISAG rats, activity of this enzyme did not differ from the corresponding values of WAG rats, although enzyme activity in the plasma of NISAG rats was significantly lower than that of WAG rats. Since NISAG rats are characterized by low activity of renin in the renal cortex, it is hypothesized that NISAG rats simulate the low-renin hypertension, in which inhibition of activity of the angiotensin-production system results from elevation of arterial pressure of central origin.
The processes of heat production in blood and bone marrow cells by method of microcalorimetry in the experiments on the rats in different terms after radiation influence were study. The irradiation of animals led to some increase of power heat energy production in bone marrow cells. The changes of heat processes in blood and bone marrow cells during month after irradiation were established.
The article is devoted to the influence of one-bran diet on functioning adrenal gland. There was investigated a level of corticosteroid and 11-dehydrocorticosterone in blood and adrenal gland rats and also aldosterone and desoxycorticosterone in adrenal gland. The consumption of one-bran diet results in increase of a corticosterone level in blood and contents of 11-dehydrocorticosterone in adrenal gland and thus is a stressful factor. The transition of animals on to a vivarium standard diet does not remove this condition completely.
Direct chromatographic method for measuring renin activity by high-performance liquid chromatography has been developed. The method is based on enzymatic hydrolysis of a new fluorescent substrate renin with formation of fluorescent angiotensin I (fAI). The content of fAI is evaluated by a calibration curve reflecting a linear relationship between the ratio of fAI and internal standard areas and the amount of resultant fA1 in reaction mixture. 100 microliters plasma is needed for analysis. After 1-h incubation at 37 degrees C the reaction mixture is introduced directly into chromatographic system with a precolumn. Acetonitrile gradient in 0.05 M Tris-TPU buffer (pH 8.0) allows a satisfactory separation of hydrolysis products. The sensitivity of the method is 100 pg fAI/ml. The method adequately reflects species characteristics of plasma renin activity and its changes caused by stimulation of renin secretion, is characterized by higher selective activity than radioimmunoassay, and is more rapid.
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The influence of the intravenously infusion of plasma substitute solution from the whey on the some indices of the lipid metabolism and the lipid peroxidation were studied in the experiments on the model of ileus. Resive data indicate the considerable alteration of the lipid peroxidation under ileus. The infusion therapy of the solution from the whey decreased the level of lipoperoxides and malondialdehyde in the liver and reduced the level of beta-lipoproteins in serum of blood.
Angiotensin-converting enzyme (ACE) activity after i.v. carbachol administration increased in the renal cortex and decreased in the renal venous plasma. Carbachol did not affect the pulmonary ACE activity. The renal ACE pool seems to be more sensitive to cholinergic effect than the pulmonary one.
Anesthetised rats with sympathetic overactivity were selected by previous testing on the base of the plasma level of corticosterone, norepinephrine and epinephrine, arterial pressure reactivity on epinephrine and acetylcholine injections, and difference between carotid and tail arterial pressure. Basal ACE activity in kidney, lung, and arterial plasma of such rats was in 5, 3 and 1.7-fold more than in mesotonic rats, respectively. I.v. administration of carbachol (10(-9) and 10(-8) mol/kg) produced decrease in arterial plasma ACE activity in dose-dependent manner (from 40 to 20 nmol/ml.min) and diminution of lung ACE activity (on 18%). It is suggested that carbachol produces an inactivation and inhibition of ACE secretion by lung and lung ACE biosynthesis in sympathetic overactivity rats. A pattern of ACE activity in plasma, kidney and lung is determined by the sympathetic-parasympathetic balance.
I.v. administration of acetylcholine in anesthetised rats with a preliminary adrenoblockade decreased the plasma renin activity (PRA) of arterial blood in rats with an increased sympathetic reactivity and a high sensitivity to acetylcholine. The PRA did not change in the rats with a high adrenergic effect on the PRA. The data suggests that the PRA response to acetylcholine depends on sympatho-parasympathetic interaction.
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The previous study demonstrated that there are two stages in acute posthemorrhagic reaction (blood loss 1.5% of body weight) when cardiac output remains low: 1) increase of lung inactivation of norepinephrine (LIN) during the first 5 min after hemorrhage; 2) decrease of LIN 10 min after hemorrhage. The present study investigated effect of captopril (1 mg/kg, i.v.) at the second stage of this reaction. Captopril prevented posthemorrhagic decrease of LIN. It is proposed that angiotensin II inhibits LIN in hemorrhage.
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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.
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.
In anesthetised rats, infusion of angiotensin II increased mean arterial pressure and inhibited the depressor responses to acetylcholine administration. Low doses of angiotensin did not exert this effect. This and other data obtained suggest that angiotensin II inhibits cardiovascular effects of the cholinergic system tonically.
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.