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Biomedical subjects

M Vigas

Publications and source records attributed to M Vigas.

At least 19 recordsLinked to original sources
PubMed1991

Evidence for immunomodulatory properties of prolactin in selected in vitro and in vivo situations.

The relationship between neuroendocrine regulation and the immune system has recently become the subject of intense investigations. The pituitary secretes both immunostimulatory (growth hormone and prolactin) and immunosuppressive (ACTH) hormones, and is thus involved in the control of immune functions. The present work was aimed at the study of the immunoregulatory properties of prolactin in selected in vitro and in vivo model situations. Prolactin was found to enhance recovery of the receptor for sheep red blood cells (in vitro). Compared with control cells, incubation with prolactin and/or prolactin containing sera significantly enhanced the capacity of trypsin treated lymphocytes from the peripheral blood of healthy volunteers to form E-rosettes. Chlorpromazine stimulated prolactin release in males, and lactation stimulated prolactin release in females raised the number of large granular lymphocytes in peripheral circulation. Sera containing elevated prolactin levels stimulated the metabolic activity of peripheral neutrophilic leukocytes. These results suggest that prolactin may stimulate selective functions of cellular immunity, and that it is involved in interactions between the nervous, the hormonal and the immune systems.

Adult↗
PubMed1991

[Radical and selective removal of hyperfunctional hypophyseal adenomas using a transsphenoidal approach].

The authors investigated the possibility of radical removal of adenomas of the pituitary (AH), while preserving remnants of pituitary tissue, in 23 patients with primarily operated hyperfunctional AH producing PRL (14 patients), STH (8 patients) and ACTH (1 patient). Normalization of the pathologically elevated hormone level was achieved by the transsphenoid operation without supplementary treatment in 13 of 16 patients with defined and in 3 of 7 patients with invasively growing AH (PRL in 10, STH in 5 and ACTH in one patient), i.e. in 69.5% Identification and preservation of remnants of the pituitary was possible in 20 patients (in all 16 with defined and in 4 of 7 with invasive AH); 17 of them (73.9%) do not need hormonal substitution. Radical and at the same time selective adenomectomy was achieved in 14 patients (60.9%) incl. three patients with invasively growing tumours. The improved activity of the pituitary is manifested clinically after successful operation in particular in young patients by improved gonadal function.

Adenoma↗
PubMed1990

Glucoreceptors located in different areas mediate the hypoglycemia-induced release of growth hormone, prolactin, and adrenocorticotropin in man.

In young male volunteers, the changes in growth hormone (GH), prolactin (PRL), and adrenocorticotropic hormone (ACTH) release in response to insulin injection combined with the infusion of saline, glucose, and fructose were evaluated. Glucose infusion in a dose which prevented insulin hypoglycemia completely abolished endocrine responses. Infusion of fructose, which is known not to cross the blood-brain barrier (BBB), did not influence the GH release during hypoglycemia; however, it inhibited PRL secretion. The ACTH response was slightly attenuated and delayed, while the hypoglycemia-induced rise in cortisol levels was not modified by fructose infusion. These data indicate that the glucoreceptors mediating the signals for a complete counterregulatory neuroendocrine response are not located in a single brain structure. Stimuli for GH release are produced in areas of the central nervous system protected by the BBB, while those for PRL release are presumably present in structures not protected by the BBB. Glucoreceptors triggering ACTH release are located both inside and outside the BBB.

Adrenocorticotropic Hormone↗
PubMed1989

Changes in blood-brain barrier function modify the neuroendocrine response to circulating substances.

It is known that various experimental, pathological and even physiological situations may be accompanied by transient increases in blood-brain barrier (BBB) permeability. The hypothesis that under such conditions the blood-borne substances can reach the active sites in the brain in concentrations high enough to influence central control of hormone release was verified in these studies. A suitable experimental model of BBB opening by protamine sulfate administration in conscious rats was introduced. Using this model it was shown that the dopaminergic blocker domperidone inhibited apomorphine-induced ACTH release if permeability of the BBB was increased, but not under normal conditions. It is suggested that the changes in BBB function can modify the neuroendocrine response also to other circulating substances and this may be an important, until now unconsidered phenomenon in neuroendocrine research.

Adrenocorticotropic Hormone↗
PubMed1989

[Central regulation of adenohypophyseal function].

The secretion of adenohypophyseal hormones is controlled by hypothalamic hypophysotropic hormones with stimulating (hormone releasing factors) or inhibitory (hormone release inhibiting factors) actions. The release of hypothalamic hormones is regulated by hierarchically higher nerve centres via neurons which liberate neurotransmitters at their endings. The secretion of growth hormone is controlled by hypothalamic hormones, somatotropin releasing factor and somatotropin release-inhibiting factor; of the neurotransmitters, the strongest effects have noradrenaline and dopamine. The release of ACTH is controlled by two stimulating hormones, the ACTH releasing factor and vasopressin, the effects of neurotransmitters are less marked, with the involvement of noradrenaline, serotonin, acetylcholine, gamma aminobutyric acid and other agents. Prolactin release is under the main inhibitory control of hypothalamic dopamine, no release-stimulating hypothalamic factor could be unequivocally demonstrated as yet; likely, several peptides are involved in this mechanism. The release of thyrotropic hormone is stimulated by thyrotropin releasing factor, whereas somatotropin release-inhibiting factor has an inhibitory action. Of the neurotransmitters, the inhibitory effect of dopamine is important; this agent however acts also at the hypophyseal level. External hypothalamic hormones and regulatory neurotransmitters are used in the diagnosis and treatment of neuroendocrine disorders.

Humans↗
PubMed1988

Apomorphine injection stimulates beta-endorphin, adrenocorticotropin, and cortisol release in healthy man.

The effect of single injections of a dopaminergic agonist, apomorphine, on pituitary-adrenocortical function was investigated in healthy adult men by the measurement of plasma ACTH, beta-endorphin, cortisol and GH immunoreactivities. Single, subcutaneous injection of a subemetic dose of apomorphine (0.75 mg) resulted in a pronounced increase in plasma concentrations of GH, as well as ACTH, beta-endorphin, and cortisol, without induction of any serious adverse drug effects. These findings were confirmed in two separate experiments.

Adrenocorticotropic Hormone↗
PubMed1988

Activation of NK cells in subjects exposed to mild hyper- or hypothermic load.

The effect of mild hyper- and hypothermic stress on release of selected hormones (somatotropin, noradrenaline, etc.), interferon (IFN), and activity of NK cells in the blood was examined in groups of young males during a 30 min exposure to 39 degrees C and 4 degrees C. A quick release of somatotropin was registered in 44% of examinees in the hyperthermic group, while the persons exposed to 4 degrees C reacted with a release of noradrenaline only. Concurrently, an elevation of NK cell activity was observed both in the subgroup releasing somatotropin after hyperthermic stress and in the group exposed to cold. Since these forms of mild stress did not lead to an appearance of IFN in the serum, the possibility of an NK cell activating effect of somatotropin and/or the adrenal hormones was tested. While the adrenal hormones stimulated the NK cell activity in vitro, no support for a similar role for somatotropin was found.

Adult↗
PubMed1988

Effect of acute cold exposure and insulin hypoglycemia on plasma thyrotropin levels by IRMA in healthy young males.

Thyrotropin (TSH) levels in plasma were estimated with the aid of immunoradiometric assay in two groups of healthy male subjects aged 21-22 years in two experiments: 1. acute (30 min) exposure to 4 degrees C in a cold room; 2. insulin (0.01 U per kg i.v.) hypoglycemia at room temperature and at 55 degrees C. Immediately after cold exposure a decrease of TSH level was found (P less than 0.01), while no changes were observed during 30 min exposure. After insulin injection a significant decrease (P less than 0.05 to less than 0.001) of TSH level was found at 45 to 120 min irrespectively of the ambient temperature. In addition, increased levels of noradrenaline and decreased levels of growth hormone after cold exposure are presented.

Adult↗
PubMed1988

Diminished growth hormone secretion in blind males after L-dopa stimulation.

Growth hormone secretion after L-dopa administration (1000 mg p.o.) was investigated in young adult normal and blind volunteers. The average increment of plasma growth hormone after L-dopa stimulation in the blind was below the criterion for a positive response (less than 5 ng ml-1). The control volunteers showed normal response. After L-dopa stimulation there was a significantly diminished growth hormone response in the young adult blind compared to control volunteers.

Administration, Oral↗
PubMed1988

Effect of human growth hormone and somatomedin on the recovery of sheep red blood cell receptor in peripheral T-lymphocytes.

The effect of growth hormone (GH) and somatomedin (SM) on the recovery of sheep red blood cell (SRBC) receptor in trypsinized human T-lymphocytes was studied either with the use of sera from patients with acromegaly or pituitary dwarfism or after the addition of exogenous GH, SM or thymosin to human sera. It was found that GH does not show any effect on the recovery of SRBC receptor, but it may act through the increase of SM level. It was concluded that the regulation of cellular immunity may be influenced by GH through its stimulatory action on the synthesis and release of somatomedins.

Acromegaly↗
PubMed1987

Effects of sauna and glucose intake on TSH and thyroid hormone levels in plasma of euthyroid subjects.

The effect of sauna on thyroid function parameters and its modification by glucose was studied in young euthyroid male volunteers. A 30-minute stay in sauna resulted in an increase in plasma TSH; the response was exaggerated if glycemia had been increased by oral glucose intake at the beginning of the experiment. Plasma rT3 also increased in sauna, this response was, however, blunted by the higher glycemia. TSH response to sauna was definitely present in young men (aged 20 to 25) and absent in middle-aged ones (50 to 55). To explore the mechanism of the effect of increased glycemia, TRH tests were performed and dopamine infusions were administered with and without glucose pretreatment. Increased glycemia did not affect TSH and T3 response to TRH in young volunteers; however, 90 minutes after the administration, plasma rT3 levels were significantly lower in glucose pretreated subjects than in those receiving TRH injections after water pretreatment. Simultaneous infusion of glucose prevented the inhibitory effect of dopamine infusion on plasma TSH. It was concluded that glucose directly modulates the effect of sauna on plasma TSH at a suprapituitary level, while the inhibiting effect of glucose on plasma rT3 response to sauna and TRH is probably mediated by the insulin effect on thyroid hormone metabolism.

Adult↗
PubMed1987

Insulin-induced hypoglycemia activates the release of adrenocorticotropin predominantly via central and propranolol insensitive mechanisms.

The dynamic patterns of pituitary-adrenocortical and sympatho-adrenal hormone responses to insulin hypoglycemia as well as the relative importance of central vs. peripheral control of hypoglycemia-induced ACTH secretion were evaluated. In conscious rats bearing indwelling cannulae, the changes in hormone concentrations after insulin injection were dependent on the changes in blood glucose levels with respect to both time course and magnitude. ACTH, corticosterone, epinephrine, and norepinephrine levels were found to be maximal at 60 min after 2.5 IU kg-1 insulin injected ip, whereas earlier (20 min) but smaller increases were obtained in response to 0.5 IU kg-1 insulin injected iv. In rats 6-7 days after lesions of the medial basal hypothalamus (MBH), the rise of ACTH during insulin hypoglycemia was markedly inhibited and corticosterone levels were significantly reduced. Simultaneously, the hypoglycemia-induced increase in plasma epinephrine was unchanged and that in plasma norepinephrine was significantly enhanced in rats with the MBH destroyed. The beta-adrenoreceptor blocker propranolol did not inhibit ACTH and corticosterone responses to hypoglycemia in either sham-operated or MBH-lesioned animals. We conclude that the main factors triggering ACTH release during insulin-induced hypoglycemia are of central rather than peripheral origin. The high concentrations of circulating catecholamines occurring during insulin hypoglycemia are not responsible for pituitary-adrenocortical activation by direct, beta-adrenoreceptor mediated action at the pituitary level.

Adrenocorticotropic Hormone↗
PubMed1986

Increased glucagon secretion during hyperthermia in a sauna.

Plasma glucagon, adrenaline, noradrenaline, insulin and glucose concentrations were measured in 7 healthy young males during hyperthermia in a sauna bath: plasma glucagon levels increased from baseline values of 127.0 +/- 12.9 (SEM) pg X ml-1 to a maximum of 173.6 +/- 16.1 (SEM) pg X ml-1 at the 20th min of exposure. No change in plasma insulin and a slight increase in plasma glucose concentration were seen. Since a concomitant moderate increase in plasma catecholamine levels was also present, the adrenergic stimulus is believed to trigger glucagon release during hyperthermia. Diminished visceral blood flow, known to occur in sauna baths, may cause a decrease in the degradation of plasma glucagon and thus contribute to the elevated plasma glucagon levels.

Adult↗