[Effect of beta-endorphin on catecholamine levels in the rat hypothalamus and cerebral cortex]. / Vliianie beta-éndorfina na soderzhanie katekholaminov v gipotalamuse i kore bol'shikh polusharii krys.

The present paper deals with the effect of beta-endorphin on catecholamine content in the hypothalamus and cerebral cortex of male rats. beta-endorphin was found to decrease catecholamine content in the rat brain, with the degree of reduction depending on the brain topography and the time following the peptide administration. 5 min later no changes in catecholamine content were observed either in the hypothalamus or in the cerebral cortex. 20 min later beta-endorphin induced a statistically significant fall of catecholamine concentration in the hypothalamus. A tendency towards its decrease was also observed in the cerebral cortex. 60 min later beta-endorphin produced an insignificant decrease in catecholamine level in both brain areas under study. It may be therefore suggested that beta-endorphin-induced decrease of catecholamine content in the hypothalamus and cerebral cortex represents one of the mechanisms underlying beta-endorphin stimulating action on a number of trophic functions of the hypophysis.

[Dynamics of the concentration of cyclic adenosine monophosphate in the tissues of rats with insulin hypoglycemia]. / Dinamika soderzhaniia tsiklicheskogo adenozinmonofosfata v tkaniakh krys pri insulinovoi gipoglikemii.

The paper is concerned with the data on the cAMP content in rat tissues 15, 30, 60 and 120 minutes after insulin injection. Rapidly developing heterogenous changes were recorded in the cAMP content of rat tissues during insulin-induced hypoglycemia and stress reaction. The evidence obtained indicates that during stress reaction the line of the changes in the entire body depends on the triggering of numerous neurohumoral mechanisms that regulate the most essential processes of body activity via the adenylate cyclase system.

[Various mechanisms of disorders of the hypothalamo-hypophyseal-adrenal system in Cushing's syndrome]. / Nejotorye mekhanizmy narusheniia gipotalamo-gifofizarno-nadpochechnikovoi sistemy pri bolezni Itsenko-Kushinga.

The authors present the results of study of corticotropine and cortizol secretion under the effect of stress caused by insulin hypoglycemia, of sensitivity of the adrenal glands to the administration of exogenous synthetic corticotropine, and of the 24-hour rhythm of the corticotropine and cortizol secretion in 26 healthy persons and in 57 patients suffering from Itsenko-Cushing's disease, including 25 after a course of treatment with chloditan, an inhibitor of the adrenal cortex function. Blood corticotropine content was determined by the radioimmunological method, and of cortizol--by competitive binding. There was revealed no significant increase of corticotropine and cortizol secretion in response to insulin hypoglycemia in Itsenko-Cushing's disease, this pointing to disturbance of the hypothalamo-hypophysio-adrenal system at the hypothalamic level. No qualitative differences were found in response of the adrenal cortex to corticotropine, this indicating the absence of changes of its sensitivity to this hormone. The 24-hour rhythm of corticotropine and cortizol secretion in this disease is inverted. At the immediate periods after chloditan treatment no normalization of the response of the adrenal cortex to insulin hypoglycemia, and of the 24-hour rhythm of corticotropine and cortizol secretion, and also of the changes in the adrenal cortex sensitivity to corticotropine was seen.

Somatotrophic, thyrotrophic and adrenocorticotrophic functions of the anterior pituitary in obesity.

The basal plasma level of GH, TSH and ACTH and the reserve capacities of the adenohypophysis in the secretion of these hormones was investigated radioimmunologically in 80 patients with excessive weight (from 15.3% to 180.0%) and a group of healthy subjects. It is shown that obesity is accompanied by diverse changes of the anterior pituitary GH, TSH and ACTH functions, which may be explained by their varied participation in the fatty metabolism. The pituitary somatotrophic function is weakened in obese subjects and its disorders advance with increase of the grade of obesity. Reduced pituitary thyrotrophic function in obesity causes weakening of thyroid function; disorders of the thyroid regulation occur at the hypothalamic level. The increased blood plasma concentration of ACTH in obese subjects has a compensatory character. The reserve capacities of the adrenocorticotrophic function of the pituitary are diminished in obestiy. Disturbances of the anterior pituitary GH, TSH and ACTH functions show a single-direction character both in alimentary-constitutional and in hypothalamic obesity.

[Somatotropic function of the pituitary gland in persons with growth disorders]. / Somatotropnaia funktsiia gipofiza u bol'nykh s zaderzhkoi rosta

The authors present the results of study of the somatotropic function of the hypophysis in 18 healthy children and in 70 patients suffering from various forms of growth retardation. The blood serum level of the STH of the hypophysis was studied by the authors by standard sets for radioimmunological determination on fasting stomach and in dynamics during the standard glucose-tolerance test. The data of basal, maximal and mean STH levels were taken into consideration. Investigations revealed a reduction of the somatotropic function of the hypophysis in the patients with hypophysial, cerebral and somatotropic nanism. With the first tow forms of growth retardation the disturbances were associated with the organic affections of the hypophysis or of the hypothalamus, and in the somatogenic one- they were functional. Somatotropic function was retained in spondylo-epiphysial dysplasia and in the patients with thyrogenic nanism given displacement therapy. In the patients with the Shereshevsky-Turner syndrome the STH secretion remained unchanged, but the reaction of the hypothalamo-hypophysial system to the functional distrubances was disturbed. An increase of the mean STH level followed complex therapy.