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Biomedical subjects

G Delitala

Publications and source records attributed to G Delitala.

At least 55 records · Page 3Linked to original sources
PubMed1987

Naloxone administration does not affect gonadotropin secretion in patients with Klinefelter's syndrome.

Plasma LH and FSH were measured every 20 min in a group of patients with Klinefelter's syndrome before and after placebo or naloxone administration (8 mg iv as a bolus followed by an infusion of 4 mg/h for 4 h) both in baseline conditions (N = 6) and during treatment with testosterone enanthate (200 mg im every two weeks; N = 4). The mean LH areas measured during saline infusion in baseline conditions (7888 +/- 758 IU/l per min mean +/- SEM) and during testosterone treatment (5042 +/- 2039 IU/l per min) were not significantly different from those measured during naloxone infusion (baseline 8317 +/- 818 IU/l per min; during testosterone treatment 5395 +/- 2007 IU/l per min). Similar results were obtained for FSH. These data suggest that in patients with Klinefelter's syndrome, the opioidergic inhibition of gonadotropin release is lacking and is not restored by testosterone replacement therapy.

Adult↗
PubMed1987

Effect of nifedipine and verapamil on carbohydrate metabolism in hypertensive patients with impaired glucose tolerance.

Intracellular Ca2+ influx is an essential step in insulin (I) release. Calcium antagonists are reported to reduce I release in vitro and in patients with impaired glucose tolerance (IGT) during acute administration. Their effects during long-term therapy are still controversial. To evaluate the effects of chronic verapamil (V) and nifedipine (N) on carbohydrate metabolism, 12 hypertensive patients (WHO II; aged 37-64 years) with IGT underwent intravenous glucose tolerance tests (IVGTT) (0.33 g/kg body weight in 3 min), arginine (A) infusion (30 g/30 min), and hypoglycemic stress (regular insulin 0.15 U/kg body weight) during which blood levels of glucose (G), I, growth hormone (GH), glucagon (IRG), and cortisol (C) were measured. The patients were then randomized to V (120 mg b.i.d.) or N (20 mg b.i.d.) treatment and, 1 month later, both IVGTT and A infusion were repeated. Hormone determinations were performed by the radioimmunoassay (RIA) and G by the enzymatic method. The patients were maintained on their usual diet for the duration of the study. The rate of decline of G during IVGTT was expressed as Conard's K coefficient (K; normal values greater than 1.3). I and GH during IVGTT were evaluated as the differences between basal and peak values. I, IRG, and GH during A infusion were analyzed as incremental areas. Our results show that neither V nor N impaired carbohydrate metabolism in hypertensive patients with IGT.

Adult↗
PubMed1986

A clinical study on the relationship between the pineal gland and the opioid system.

Recent reports point to a link between the pineal gland and the opioid system. In order to investigate this relationship, two separate studies were performed on humans. Beta-endorphin plasma levels were determined after melatonin administration (0.2 mg/kg b.w. i.m. at 2 p.m.). Melatonin serum values were evaluated after administration of FK 33-824, a met-enkephalin analogue (0.3 mg i.v. infusion at 9 a.m.). A significant decrease of beta-endorphin plasma levels was observed 120 minutes after melatonin injection. Melatonin release was stimulated by FK 33-824, with a peak at 30 minutes. The present results provide evidence of the inhibitory effect of melatonin on beta-endorphin secretion and the stimulatory action of the opioid peptides on the pineal gland. However, further studies will be required to clarify the relationship between the opioid system and the pineal gland.

Adolescent↗
PubMed1986

An analogue of met-enkephalin attenuates the pituitary-adrenal response to ovine corticotrophin releasing factor.

The met-enkephalin analogue, DAMME, suppresses the pituitary-adrenal axis in normal subjects; it is not clear whether this occurs at the level of the pituitary or above. We therefore administered synthetic ovine corticotrophin releasing factor (CRF-41) 100 micrograms i.v. to a group of normal male subjects, with or without pretreatment with DAMME 250 micrograms i.v., and monitored the response of plasma ACTH and serum cortisol. CRF-41 caused a marked stimulation of ACTH and cortisol release, but this was significantly attenuated by pretreatment with DAMME. It is therefore concluded that DAMME either directly inhibits the corticotroph at the level of the pituitary, or that it suppresses release of an additional factor which normally potentiates the action of CRF-41 on the pituitary.

Adolescent↗
PubMed1986

Effect of adrenergic antagonism on the growth hormone, prolactin and cortisol response to a synthetic opioid agonist in man.

The intravenous administration of 250 micrograms D-Ala2-MePhe4-Met-enkephalin-O-ol (DAMME) caused a marked increase in circulating growth hormone (GH) and prolactin (PRL), and a fall in cortisol, in 14 normal subjects. Neither the alpha 1-antagonist thymoxamine, nor the alpha 2-antagonist yohimbine, significantly altered the GH and PRL responses to DAMME, suggesting that in man the growth hormone- and prolactin-releasing effects of exogenous opioids are not mediated through adrenoceptor pathways. The fall in cortisol induced by DAMME was not affected by thymoxamine, but was significantly attenuated by yohimbine, indicating that opioids may lower circulating cortisol via an interaction with noradrenergic pathways.

Adult↗
PubMed1986

Naloxone administration does not affect gonadotropin secretion in agonadal men either basally or during testosterone treatment.

Naloxone administration has no effect on plasma gonadotropin levels of agonadal men. The present study was designed to evaluate whether testosterone replacement therapy could restore LH responsiveness to naloxone in such men. We measured plasma LH and FSH levels at 15-min intervals during naloxone infusion (8 mg in 1 min followed by 12 mg in 3 h) and for the following 3 h in a group of agonadal men both before and after at least 2 months of three different schedules of testosterone replacement therapy: 1) testosterone undecanoate, 40 mg three times a day by mouth; 2) testosterone enanthate 200 mg im every 2 weeks; and 3) testosterone enanthate 100 mg im once a week. Mean plasma gonadotropin levels as well as LH pulse frequency did not vary during naloxone infusion vs. placebo either basally or during each testosterone regimen. These results suggest that long term testosterone therapy does not affect the altered opioid modulation of gonadotropin secretion which is present in agonadal men.

Adolescent↗
PubMed1985

Naloxone administration does not affect gonadotrophin secretion in male patients with isolated hypogonadotrophic hypogonadism.

We evaluated the gonadotrophin response to acute naloxone administration (10 mg iv) in 4 male patients with isolated hypogonadotrophic hypogonadism (age range 18.5-26 years) before and after pituitary priming with daily infusions of GnRH (25 micrograms/h for 4 h) for 4 days. A blunted gonadotrophin response to acute GnRH administration (100 micrograms iv) and a lack of response to naloxone was observed before pituitary priming. After repeated infusions of GnRH, pituitary gonadotrophin responsiveness to GnRH was restored, whilst naloxone still did not affect gonadotrophin levels. Our data suggest that in male isolated hypogonadotrophic hypogonadism 1) the lack of pituitary response to naloxone is not due to pituitary hyporesponsiveness to GnRH; 2) endogenous opioids do not exert any inhibitory influence on GnRH secreting neurons and thus are not involved in the pathogenesis of this disease.

Adult↗
PubMed1985

Effects of naloxone infusion on gonadotrophin and prolactin concentrations in patients with chronic renal failure.

Serum prolactin, luteinising hormone and follicle-stimulating hormone, determined by radioimmunoassay were measured during the infusion of 10mg naloxone or saline in eight male patients with chronic renal failure on regular dialysis and in seven normal controls. Neither saline nor naloxone caused any significant change in luteinising hormone, follicle-stimulating hormone or prolactin in patients with chronic renal failure. On the contrary, luteinising hormone secretion was significantly stimulated by naloxone in normal controls. Since naloxone is a specific antagonist of opiate receptors, the results would suggest a reduced hypothalamic opiate tone in patients with chronic renal failure. The data does not support the concept that the high circulating met-encephalin reported in chronic renal failure represents the pathogenetic cause of hyperprolactinaemia in chronic renal failure.

Adult↗
PubMed1984

Effects of different dopaminergic antagonists on bromocriptine-induced inhibition of norepinephrine release.

In this study we evaluated the effects of placebo or acute bromocriptine (BC) administration (2.5 mg orally) on plasma catecholamines, systolic and diastolic blood pressure (BP), heart rate, and plasma PRL in six normal subjects [group I, mean age 33.2 +/- 5.4 (SD) yr] in the supine as well as upright position. BC induced a significant decrease in plasma norepinephrine in the supine [167.7 +/- 16.8 (SEM) vs. 101.9 +/- 33.7 pg/ml, P less than 0.005] and upright positions [397.3 +/- 27.7 vs. 211.3 +/- 26.7 pg/ml, P less than 0.005], a decrease in systolic and diastolic BP and a decrease in plasma PRL (P less than 0.01). After standing, epinephrine levels increased significantly (53.6 +/- 11.8 vs. 226.4 +/- 71.0 pg/ml, P less than 0.05). The study was repeated in a second group of seven normal subjects (mean age, 32.3 +/- 12.9 yr) after placebo or metoclopramide (20 mg orally) plus BC. In this group metoclopramide, a central and peripheral antidopaminergic agent, counteracted the BC-induced effects found in group I, both in the basal and stimulated conditions. Plasma PRL increased significantly (P less than 0.025). Finally, to assess the effect of peripheral dopaminergic blockade on BC-induced changes in sympathetic outflow, we repeated the study in seven normal subjects (group III, mean age, 30.1 +/- 5.0 yr) after placebo or domperidone (20 mg orally) plus BC. Domperidone blocked the effects of BC on norepinephrine and BP in the supine position. On standing there was a significant decrease in systolic (P less than 0.05) and diastolic (P less than 0.05) BP and an increase in epinephrine levels (58.9 +/- 12.2 vs. 109.8 +/- 24.6 pg/ml, P less than 0.05) was still observed. Plasma PRL increased significantly (P less than 0.025). The results of this study suggest that the inhibition of sympathetic outflow induced by BC is peripherally mediated. As peripheral dopamine receptor blockade did not counteract all the effects after BC during standing, dopaminergic modulation of central reflex sympathetic activation is suggested.

Adult↗
PubMed1984

Effects of naloxone on catecholamine plasma levels in adult men. A dose-response study.

To evaluate a possible role for endogenous opiates in modulating sympathetic-adrenal function in humans, we measured plasma epinephrine and norepinephrine (radioenzymatic method), blood pressure and heart rate in 8 normal men (aged 24-33 years) before and after placebo or different doses (0.4, 4.8, 10 mg) of naloxone. In 6 subjects plasma insulin and glucagon levels were also measured by radioimmunoassay after placebo and 10 mg naloxone. Naloxone had no significant effect upon blood pressure, heart rate, plasma insulin, glucagon or norepinephrine. Placebo, 0.4 and 4.8 mg naloxone caused no significant change in peripheral levels of epinephrine while 10 mg produced an increase in epinephrine concentrations 15 min after iv injection (186 +/- 23 vs 99 +/- 9 pmol/l, P less than 0.01). Since naloxone did not modify plasma levels of insulin and glucagon, an indirect effect of naloxone on adrenal medullary secretion seems to be excluded. These results are in agreement with in vitro experimental data obtained in animals and suggest that endogenous opiates also have a role in modulating adrenal medullary secretion in man.

Adrenal Medulla↗
PubMed1983

Effects of naloxone infusion on basal and breast-stimulation-induced prolactin secretion in puerperal women.

The effects of naloxone infusion on plasma prolactin (PRL) levels and on the PRL response to mechanical breast emptying were investigated in a group of puerperal women, Five, 10, and 20 mg naloxone administered to women on days 2 to 3 of the puerperium produced no significant change in serum PRL. The same dose of naloxone had no significant effect on serum PRL response to mechanical breast stimulation in puerperal women. The results suggest that endogenous opioid peptides are not major modulators of PRL secretion in the puerperium.

Adult↗
PubMed1983

The participation of hypothalamic dopamine in morphine-induced prolactin release in man.

In order to assess the role of dopamine in opiate-induced prolactin secretion, morphine alone or in combination with the dopamine blocker metoclopramide, or the L-aromatic aminoacid decarboxylase inhibitor benserazide, was administered to a group of normal adult men. Morphine (10 mg) stimulated prolactin release in all subjects; however, the effect was totally abolished when 10 mag metoclopramide or 200 mg benserazide were given before the opiate agonist. The prolactin releasing effect of a sub-maximal metoclopramide dose (1 mg) was potentiated by morphine. In vitro, benserazide was totally inactive in stimulating prolactin release by isolated anterior pituitary cells. Moreover, benserazide failed to alter the inhibiting action of dopamine on prolactin release. The data suggest that opiates stimulate prolactin release in man by acting through dopaminergic mechanisms.

Adult↗
PubMed1983

Opiate peptides control growth hormone through a cholinergic mechanism in man.

Opiate peptides are known to elevate circulating GH in man, and data in other animals suggest that acetylcholine may be involved. We have administered the long-acting met-enkephalin analogue DAMME to 6 normal males, and have shown that the resulting elevation in GH is blocked by the specific cholinergic antagonist, pirenzepine. It seems likely that a cholinergic mechanism may interact with opiate-induced changes in GH in man.

Adult↗
PubMed1983

Differential effects of opiate peptides and alkaloids on anterior pituitary hormone secretion.

In order to investigate the opiate receptors involved in the control of anterior pituitary hormone secretion, five different opioid drugs were administered intravenously to groups of 6 normal male subjects. Morphine (10 mg), methadone (10 mg), pentazocine (30 mg), nalorphine (10 mg) and 0.25 mg of the met-enkephalin analogue, DAMME, all caused similar increases in circulating prolactin with falls in serum LH and cortisol. Methadone and DAMME also elevated GH and TSH; morphine elevated TSH but not GH, nalorphine GH but not TSH. After pentazocine neither GH nor TSH changed. FSH failed to change significantly after any drug. All these changes, except serum cortisol, were antagonised by 4 mg naloxone. Taking into account the known receptor subtypes preferentially activated by each opiate, it is suggested that prolactin secretion is modulated by epsilon-receptors and TSH by mu-receptors. The control of ACTH probably involves delta-or kappa-receptors, that for LH kappa-or epsilon-receptors. It is not possible on present data to allocate a specific receptor mediating the opioid control of GH.

Adult↗
PubMed1983

On the role of dopamine receptors in the naloxone-induced hormonal changes in man.

To assess the role of dopamine receptors in naloxone-induced hormonal changes, the effects of dopamine and metoclopramide on anterior pituitary hormone secretion were studied during the infusion of the opiate blocker in normal men. Naloxone stimulated LH and cortisol secretion in all subjects, whereas FSH, TSH, PRL, and GH did not change. The infusion of dopamine completely suppressed the naloxone-induced LH rise; on the contrary, metoclopramide failed to alter the magnitude of the increments in LH observed during the infusion of the opiate blocker. The cortisol response to naloxone remained unchanged during dopamine and metoclopramide infusion. Metoclopramide stimulated PRL and TSH release during naloxone treatment, whereas dopamine suppressed PRL and TSH secretion. The data do not suggest a participation of dopamine receptors in the naloxone-induced hormonal changes in man and confirm a suppressive effect of dopamine infusion on LH release in humans.

Adult↗