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Biomedical subjects

M Vigas

Publications and source records attributed to M Vigas.

At least 109 records · Page 6Linked to original sources
PubMed1983

Immediate increase of thyroid hormone release during acute stress in rats: effect of biogenic amines rather than that of TSH?

An increase of thyroxine (T4; 36% in average) and 3,5,3'-triiodothyronine (T3; 9% in average) levels in plasma was found in rats after 2 min of immobilization stress (IMO), while later (from 5 to 240 min of IMO) the level of both hormones decreased sharply. This increase was prevented by ip injection of phenoxybenzamine (4 or 16 mg kg-1), prazosin (2.5 mg kg-1), yohimbin (4 or 16 mg kg-1) and fluoxetine (10 mg kg-1) at 60 min before IMO, but similar injections of phentolamine (4 or 16 mg kg-1), tolazoline (4 or 16 mg kg-1), methysergide (10 mg kg-1), cyproheptadine (10 mg kg-1) as well as of lower doses of prazosin (0.6 or 1.2 mg kg-1) did not show such an effect. The level of TSH was increased after 2 min IMO too, but this was considered to be a separate phenomenon from the increase of T4 and T3, since in several groups injected with some of the above drugs the level of TSH was decreased together with increased levels of T4 and T3. It is suggested that the acute release of thyroid hormone might be due to the effect of biogenic amines which may be blocked by some alpha-adrenergic blocking agents. Since neither adrenalectomy nor adrenal-medullectomy prevented such a release, it may be concluded that circulating catecholamines of adrenal origin did not play any role in this process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1983

Adenopituitary hormone response to exercise combined with propranolol infusion in man.

The effect of non-selective beta-blocker propranolol on the changes of plasma GH, prolactin and cortisol level during physical exercise in healthy untrained men has been evaluated. Acute i.v. pretreatment with propranolol resulted in an increased response of plasma GH level to the exercise on a bicycle ergometer. Propranolol significantly potentiated also the response of plasma cortisol level to submaximal exercise. No changes in urinary excretion of free cortisol and 17-OHCS during exercise combined with propranolol infusion as compared to that during exercise alone were observed. The increase of plasma prolactin level after exercise was not altered by propranolol administration. It is suggested that central beta-adrenoreceptors may play an inhibitory role in the control of GH and ACTH secretion during exercise. However, the interaction of propranolol with other central neurotransmitters as well as its peripheral effects, particularly the reduction in physical performance, must also be taken into consideration.

Adult↗
PubMed1982

ACTH and corticosterone response to naloxone and morphine in normal, hypophysectomized and dexamethasone-treated rats.

The effect of opiate receptors blocker naloxone on ACTH and corticosterone secretion in normal, dexamethasone-treated and hypophysectomized rats was studied. A dose-related increase in plasma corticosterone level was found at 45 min after s.c. injection of naloxone in a dose range of 0.25-2.0 mg kg-1. The rise in plasma corticosterone was preceded by a slight increase in plasma ACTH. Acute morphine administration in a relatively low dose (6 mg kg-1 s.c.) induced a significant rise in both plasma ACTH and corticosterone levels. Dexamethasone treatment was followed by low basal corticosterone level, by total inhibition of the stress response and response to morphine injection, while the response to ACTH administration was normal. Under these circumstances as well as in rats 6 days after hypophysectomy, naloxone failed to increase plasma corticosterone levels. It is concluded that a direct stimulation of corticosteroid biosynthesis in adrenal cortex is not involved in the mechanism of naloxone-induced activation of pituitary-adrenocortical function.

Adrenocorticotropic Hormone↗
PubMed1982

Plasma testosterone during bicycle ergometer exercise without and after L-dopa pretreatment.

The level of testosterone in plasma during submaximal, prolonged submaximal and maximal exercise on a bicycle ergometer was measured in healthy untrained men. To evaluate the possible involvement of prolactin in the regulation of testosterone secretion during exercise, the influence of prolactin inhibition by oral L-dopa (1 g) pretreatment was also studied. The exercise evoked a small but significant rise of testosterone concentration with peak levels immediately at the end of work performance or 10 min after that. No substantial difference between the response to submaximal and maximal exercise was noted. In these experiments the findings by others on a lack of plasma LH changes and significant increase of plasma prolactin were confirmed. Pharmacological blockade of prolactin release by L-dopa pretreatment failed to modify the response of testosterone to bicycle ergometer exercise. It may be suggested that prolactin is not involved in the induction of plasma testosterone increase during physical exercise.

Adult↗
PubMed1982

Effect of growth hormone on the metabolic activity of phagocytes of peripheral blood in pituitary dwarfs and acromegaly.

The increase of metabolic activity pf phagocytes estimated by nitrozolium reductase activity is often employed to distinguish between bacterial and non-bacterial febrile disorders. However, false responses has been also observed. The possible role of serum growth hormone in the activation of tetrazolium reductase activity in patients with pituitary nanism or acromegaly was studied. In isolated peripheral granulocytes of pituitary dwarfs the reductase activity was low at resting conditions as well as after starch stimulation of phagocytosis. Two hours after i. m. administration of human growth hormone the resting and stimulated tetrazolium reductase activity was significantly increased (P less than 0.05, and P less than 0.01, resp.). The increase of both activities was found also in patients with active acromegaly. A moderate increase of tetrazolium reductase activity was observed after adding of growth hormone to isolated granulocytes in vitro (P less than 0.01). These results suggest the stimulatory role of growth hormone in regulation of respiratory burst activity of peripheral granulocytes.

Acromegaly↗
PubMed1981

Activity of the sympathetic-adrenomedullary system in rats after space flight on the Cosmos biosatellites.

The indicators of adrenomedullary activity (catecholamine content (CA) and the activity of the catecholamine-synthesizing enzymes tyrosine hydrozylase (TH) and dopamine-beta-hydrozylase (DBH) were measured in the adrenal glands of rats living in a state of weightlessness for 18.5-19.5 days on board the biosatellites COSMOS 936 and COSMOS 1129. None of these indicators was significantly changed by space flight, neither in the group living in a state of weightlessness nor in the group living in a centrifuge on board the spacecraft and exposed to artificial gravity of 1 g (COSMOS 936). Animals exposed after space flight to repeated immobilization stress on Earth showed a significant decrease of adrenal adrenaline and an appreciable increase in adrenal TH activity compared to stressed animals which were not in space. These results suggest that a prolonged state of weightlessness during space flight does not by itself represent an intensive stressful stimulus for the adrenomedullary system but potentiates the response of cosmonauts to stress after return to Earth.

Adrenal Medulla↗
PubMed1981

Thyroliberin (TRH) induced growth hormone (GH) release: test of maturation of hypothalamo-pituitary axis in postnatal rat.

Small doses of TRH elicit GH release from rat pituitary provided the pituitary lacks CNS influences (e.g. in vitro or in ectopic pituitaries). We have found previously that hypothalamic regulation of TSH secretion matures between the 5th and 12th postnatal day. Therefore the possibility of TRH induced GH release was investigated in neonatal rats. GH concentration was measured by RIA at 10 min after s.c. TRH administration (4.1 pmol g-1 BW) into female Wistar rats at the age 3, 9, 12, 15, 21, 30 and 100 days. Control animals were injected the same volume (1 microliter g-1 BW) of saline. Serum GH in saline treated animals gradually decreased during postnatal ontogenesis. The TRH induced increase of serum GH level decreased during maturation: the most marked response was found at 3 days, it was somewhat lessened but still significant at 9 days and was absent in 12, 15, 30 days old and adult animals. Surprisingly, in 21 days old animals the increase of GH after TRH administration was again present. We conclude that the ability of TRH to elicit GH release in newborn rats may depend on the maturity of the hypothalamo-pituitary axis. The effect of hypothalamic somatostatin is likely to inhibit such a response at the pituitary level in older rats.

Animals↗
PubMed1981

Inhibition of stress induced hyperglucagonemia by administration of glucose in normal and alloxan-diabetic rat.

The increase in plasma pancreatic glucagon which is known to occur under several stress conditions was confirmed in fed and 18 h prefasted rats subjected to a low, "stress producing" dose of the Noble-collip drum procedure (400 revolutions per 400 s). A single dose of exogenous glucose ( 1 g kg-1) injected 3 min and 20 s before stress into the jugular vein of intact fasted or fed animals anesthetized with pentobarbital 930 mg kg-1) completely abolished their hyperglucagonemic response in stress. In alloxan-diabetic hyperglycemic rats the stress-hyperglucagonemia was exaggerated, but was also suppressible by exogenous glucose. It was concluded that: 1. the stress induced hyperglucagonemic response of both intact and alloxan-diabetic rats was completely suppressible by administration of i.v. bolus of exogenous glucose; 2. the site inhibiting effect of glucose might be located either at the level of A cell or at the level of "'glucoreceptors" in hypothalamus.

Animals↗
PubMed1980

Cerebral hypoperfusion as a stimulus for growth hormone release in man.

In healthy male volunteers the effect of a short-term cerebral ischemia due to an acute orthostatic hypotension, on the release of growth hormone (HGH) was studied. Peroral administration of guanethidine 12.5 mg t.i.d. for 3 days plus 25 mg before the experiment was used to block peripheral vascular reflexes and thus to provoke orthostatic intolerance. An extreme increase of HGH serum levels (on average from 0.8 to 13.6 ng/ml; p < 0.001) was found in subjects who developed clinical signs of syncope after assuming upright posture. The possible mechanisms of this finding are discussed.

Adult↗
PubMed1980

Decreased plasma cortisol response to pharmacological stimuli after glucose load in man.

The influence of glucose administration on plasma cortisol level after its elevation by pharmacological and physiological interventions in healthy male volunteers was studied. The increase of plasma cortisol after 1 g of L-dihydroxyphenylalanine (L-dopa) failed to be significant. However, after a concomitant oral administration of 100 g glucose, a fall of cortisol level significant also vs. initial control values was observed. The infusion of beta adrenergic blocking agent (propranolol) enhanced the cortisol response to physical exercise. However, the glucose given before propranolol infusion abolished the enhancement of cortisol response induced by this drug. The mechanism of the inhibitory effects of glucose remains to be elucidated.

Adult↗
PubMed1980

Effect of endogenous GH secretion during hyperthermic bath on glucose metabolism and insulin release in man.

In healthy male subjects the hyperthermic water bath (40 degrees C for 30 min) induced an increase of growth hormone (GH) level in plasma with the increment higher than 5 ng ml-1. One group of six good GH responders--with the mean increment of 10.9 +/- 1.67 ng ml-1 was given glucose per os immediately after the bath. In other experiment the oral glucose tolerance test (GTT) was performed in six good GH responders (mean increment 16.1 +/- 2.0 ng ml-1) at 90 min after the peak of GH increase. In both experiments the insulin release and glucose tolerance did not differ from the results obtained in the same group in a control isothermic water bath at 30 degrees C. It is concluded that endogenous increase of GH in healthy subjects did not affect the insulin secretion and disappearance of glucose from peripheral blood.

Adult↗
PubMed1979

Effect of growth hormone on acute glucagon and insulin release.

The aim was to clarify whether or not sudden spike concentrations of plasma growth hormone (GH) can affect the endocrine pancreas in vivo. The peaking of GH was reproduced by an injection (10 mg/kg iv) of bovine GH to anesthetized normal, pancreatectomized, and alloxan-diabetic dogs. In portal but not in peripheral blood, immunoreactive plasma glucagon (IRG), glucagon-like activity (GLI), and immunoreactive insulin (IRI), were significantly elevated within 10 min in normal and alloxan-diabetic dogs. In pancreatectomized dogs, GH did not affect either IRG or GLI. When a physiological dose of GH (6 microgram/kg) calculated to produce ambient peak plasma concentrations of 40 ng/ml was given to four conscious, normal dogs with indwelling portal catheters, a rise of IRG from 108 +/- 19 to 170 +/- 17 pg/ml and of IRI from 20 +/- 12 to 67 +/- 19 muU/ml (mean +/- SE) occurred within 2 min. GLI was not affected. Thus a sudden rise in GH concentration can stimulate the release of a) GLI in the presence but not in the absence of the pancreas, and b) pancreatic IRG and IRI but not extrapancreatic IRG.

Animals↗
PubMed1979

Effect of adrenergic receptor blockade on cortisol and GH response to insulin-induced hypoglycemia in man.

The effect of several drugs presumably influencing central catecholaminergic receptors on plasma cortisol and GH response to insulin-induced hypoglycemia was studied in healthy adult males. The intravenous infusion of alpha-adrenergic blocking agents tolazoline or phentolamine supressed plasma cortisol and GH response to insulin-induced hypoglycemia. After an infusion of beta-adrenergic antagonist propranolol both hypoglycemia and rise in plasma cortisol and GH were prolonged. Finally, the administration of dopaminergic blocker pimozide failed to affect the plasma cortisol response, but slightly suppressed the enhancement of GH release during hypoglycemia. Caution is recommended before making suggestions about neuroendocrine regulations from the data obtained after systemic administration of drugs. Nevertheless, it may be concluded that the hypothesis on the inhibitory role of the central alpha-adrenergic system on ACTH secretion suggested in rats and dogs was not confirmed by our results obtained in man.

Adult↗