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Biomedical subjects

K F Korovin

Publications and source records attributed to K F Korovin.

At least 19 recordsLinked to original sources
PubMed1990

[Neuroendocrine aspects of the pathogenesis and treatment of disseminated sclerosis and lateral amyotrophic sclerosis].

Comparative study of neurologic, immunologic, and endocrinologic signs of disseminated sclerosis and lateral amyotrophic sclerosis was carried out by radioimmunoassay, monoclonal antibodies, and microcytotoxic Terasaki's test. The data have shown a tendency to hyperthyroid and hypocorticoid states in 60 percent of lateral amyotrophic sclerosis patients. Fluctuations in hormonal levels of disseminated sclerosis patients were quite the opposite in 37.5 percent of cases. Thyrotropic hormone content was rarely changed (in 20 and 18.75 percent of cases, respectively), this permitting a conclusion on the possibility of an extrahypophyseal (thymic) effect on the thyroid in these conditions and on the advisability of using thyrotropin- and corticotropin-releasing hormones (8-arginine-vasopressin) in combined therapy thereof.

Adult↗
PubMed1988

[Indices of the body's neurohumoral activity and hemodynamic types in hypertension].

A study of neurohumoral parameters in patients with essential hypertension and different hemodynamic types demonstrated different patterns of hormonal change in patients with hyperkinetic, eukinetic and hypokinetic hypertension. Elevated blood tri-iodothyronine and thyroxine, seen in patients with hyperkinetic hemodynamic type, and increased catecholamine excretion in patients with hypokinetic hemodynamics may be indicative of the pathogenetic significance of the hormones in question for the formation of respective variants of essential hypertension.

Adult↗
PubMed1988

[Psychological and psychosomatic prerequisites for the development of duodenal peptic ulcer].

Altogether 276 male patients with duodenal ulcer (DU), 45 with the preulcerative condition (PUC) and 70 with gastroduodenitis were examined. Anxiety-depressive disorders were most frequently revealed in all the groups. The frequency of hypochondriac fixation in DU increased. The neurohormonal "basis" of affective rigidity is formed during PUC. Specific variants of neurohormonal rearrangement in the transformation of PUC into DU were revealed in depressive, anxiety and hysterical manifestations.

Adaptation, Psychological↗
PubMed1987

[Regional changes in circulation in response to stimulation of beta-adrenergic receptors with isoproterenol].

The muscle and adrenal fractions of cardiac output increased after injection of isoproterenol. The relative blood flow increase in skeletal muscles was accompanied with the increase in regional by-pass blood flow. The latter or reduction in the vessel permeability were found in the lungs. The cardiac output fractions decreased in extensive areas of skin, brain, myocardium, internal organs of hepatic portal vein, kidneys, testicles. The signs of the blood flow increase were found in the brain, myocardium, liver. The relative blood volume decreased in the majority of internal organs and tissues while increasing in the liver.

Animals↗
PubMed1985

[Myocardial blood supply under different degrees of emotional excitation and the pathophysiological characteristics of the mechanisms of its adaptation].

Emotional stress was stimulated by placing rats in a tight cage (moderate stress) or fixing them rigidly on a bench (marked stress) for 1 hour. In moderate emotional stress, the coronary fraction of cardiac output and effective myocardial blood supply declined considerably. Marked emotional stress caused a similar reduction in the cardiac output coronary fraction, whereas effective myocardial blood supply was not reduced, but, on the contrary, tended to increase. The decrease in coronary fraction was not related to adrenergic effects. Marked emotional stress provoked regional changes in the resistance, microcirculatory and capacity components of the vascular bed, an adaptation to enable effective myocardial blood supply and enhance cardiac activity. It was accompanied with kallikrein-kinin activation.

Adaptation, Physiological↗
PubMed1984

[Indices of thyroid activity in patients with breast cancer].

An all-round study established thyroid dysfunction in 51 reproductive, climacteric and menopausal patients with primary T2-3 NO-1 MO cancer of the breast. Hypothyroidism is attributed to functional derangement of the thyroid and disorder development in peripheral metabolism.

Adult↗
PubMed1983

[Changes in the systemic and regional circulation responses to immobilization stress in the rat after pharmacological sympathectomy].

A preliminary pharmacological desympathization (pirroxan, obzidan, ornid) decreased blood pressure, heart rate, cardiac output, and increased total vascular resistance in immobilized rats. The fraction of cardiac output decreased in lung (bronchial blood flow), liver and myocardium and increased in other organs and tissues. Relative blood supply increased in expansive regions of the skin, muscles and splanchnic organs but decreased in the liver. Opposite changes of transcapillary permeability were found in vascular regions of the skin and skeletal muscles as well as in splanchnic organs.

Animals↗
PubMed1982

[Hypophyseal-adrenal system function in disseminated breast cancer].

The functional condition of the pituitary-adrenal system was studied in 94 patients with disseminated breast cancer. A decreased excretion of 17--OCS's with urine and an increased cortisol level in blood were observed. This was interpreted as relative (extra-adrenal) failure of pituitary-adrenal function in breast cancer patients. Measures of long-term therapy (adaptogens, vitamins and hepatotropic preparations) are recommended.

17-Hydroxycorticosteroids↗
PubMed1981

The functional role of the noradrenergic neurons in the thermoregulatory circuits in mice.

Intracerebroventricular (i.c.v.) treatment of mice with 6-hydroxydopamine (6-OHDA; 20--50 micrograms per mouse), which depletes brain noradrenaline (NA) and DA, completely prevents or significantly diminishes the hypothermic effect of various classes of drugs: dopaminomimetics--apomorphine (0.5--10 mg/kg), piribedil (40--100 mg/kg), bromocriptine (3 to 10 mg/kg), CM 29-712 (2--10 mg/kg), d, l-amphetamine (1--2 mg/kg), and L-DOPA (10--100 mg/kg) in combination with Ro 4-4602 (5--40 mg/kg); cholinomimetics--oxotremorine (0.04--0.05 mg/kg), arecoline (5--10 mg/kg) and pilocarpine (2--3 mg/kg); neuroleptics--chlorpromazine, promazine, perphenazine, chlorprothixene, haloperidol, fluanisone (5--10 mg/kg); central alpha-adrenoblocker aceperone (20--40 mg/kg); inhibitor of tyrosine-hydroxylase alpha-methyltyrosine (200--300 mg/kg); inhibitor of dopamine-beta-hydroxylase--disulfiram (150--250 mg/kg) and FLA-63 (15--25 mg/kg). This antihypothermic effect was demonstrated up to 3 months after administration of 6-OHDA for DA-mimetics and neuroleptics and up to 3 weeks for cholinomimetics. The hypothermic effect of presumable GABA-mimetics Phenybut (100--150 mg/kg) and Lioresal (10--25 mg/kg) was enhanced by a prior 6-OHDA treatment. Pretreatment of mice with desipramine (25 to 30 mg/kg i.p.), protriptyline (20 mg/kg) or AW 15(1)1129 (15--20 mg/kg) 20--45 min before 6-OHDA administration protects the central NA-ergic neurons from a destructive effect of 6-OHDA and partially or completely counteracts the antihypothermic as well as prohypothermic (in the case of GABA-mimetics) effect of 6-OHDA. In rats desipramine counteracted antihypothermic effect of 6-OHDA in the case of piribedil, but not of apomorphine. Intracerebroventricular treatment of mice with a low (15 microgram) dose of 5, 6-dihydroxytryptamine (5, 6-DHT) enhanced the hypothermic effects of DA-mimetics; higher doses of 5, 6-DHT (26 and 30 micrograms) and 5, 7-DHT (40 and 46 micrograms) diminished the hypothermic effects; the antihypothermic effect of 6-OHDA was stronger than that of equimolar doses of 5, 6- or 5,7-DHT; desipramine pretreatment counteracted antihypothermic effects of 5, 6-DHT and 5, 7-DHT as well as depletion of brain NA they produce. The data presented reveal the key position for NA-ergic neurons in a temperature regulation and, particularly, in effects of various drugs on body temperature in mice. The tentative fragment of the neuronal thermoregulatory circuit is proposed in attempt to account for the presented an other known data concerning drug action (and interactions) on core temperature in mice.

Animals↗
PubMed1980

[Role of hypothalamic monoaminergic structures in regulating sympatho-adrenal system function].

The effect of pharmacological destruction of hypothalamic monoaminergic terminals on the basal and cold stress-induced secretion of neurohormones of the sympathoadrenal system (SAS) in rats was studied. The data obtained on biochemical and histochemical analysis of the hypothalamus (dopamine, noradrenaline and serotonin level, the picture of catecholaminergic terminal fluorescence) were compared with adrenaline and noradrenaline content in blood. It is assumed that function of the SAS is inhibited by hypothalamic noradrenaline and stimulated by dopamine and serotonin under cold stress.

5,6-Dihydroxytryptamine↗
PubMed1978

[Cock fighting as a model of emotional stress].

Aggressive and passive roosters displayed agonistic behaviour towards each other. The formers revealed a highly agonistic attitude in the first half of the experiment followed by an obvious decline. The passive roosters revealed a relatively stable agonstic attitude. The electrocardiorhythmograms showed that handling of the roosters and other manipulations masked the heart primary response to cock-fighting, and that the analysis of the heart rate during restitution only helped to estimate their emotional tension during fighting. Positive correlations between the aggressiveness and noradrenaline content in the plasma, were obtained. The latter correlated with the sexual activity as well. The agonistic behaviour entailed an insignificant activation of the adrenals.

11-Hydroxycorticosteroids↗