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Biomedical subjects

C Barbieri

Publications and source records attributed to C Barbieri.

At least 73 records · Page 4Linked to original sources
PubMed1983

Dopaminergic control of gastric acid and gastrin secretion in man: lack of effects after acute oral administration of ibopamine, an analogue of dopamine.

The effect of oral administration of the dopaminergic drug, ibopamine, at the dose of 200 mg and 400 mg, on basal and submaximal pentagastrin (0.25 microgram kg-1 h-1) stimulated gastric acid secretion as well as basal serum gastrin concentration has been evaluated in 24 healthy individuals. In comparison with placebo no significant changes were observed in all the variables studied. The lack of effects on gastric acid secretion might be due to a selective stimulation of dopaminergic receptors not active in the regulation of gastric acidity or not present in gastric mucosa, while unchanged serum gastrin secretion is possibly due to a poor crossing of blood-brain barrier by ibopamine.

Adult↗
PubMed1983

Effect of fenfluramine on prolactin secretion in obese patients: evidence for serotoninergic regulation of prolactin in man.

The present investigation was carried out to study the effect of serotoninergic stimulation on prolactin (PRL) secretion in man. Fenfluramine (60 mg, orally), an anorexiant drug which under acute circumstances stimulates the serotoninergic system, was administered to eight obese patients. Compared with placebo, drug administration increased PRL significantly (P less than 0.05 at 180 and 300 min, P less than 0.01 at 240 min). No significant changes were observed after fenfluramine in blood pressure, plasma aldosterone (PA), plasma cortisol, plasma renin activity, serum electrolytes or growth hormone. Since it has been reported that dopaminergic blockade raises PA concentration, the lack of change in PA in obese patients treated with fenfluramine suggests that the observed increase in PRL induced by fenfluramine is likely to be mediated by serotoninergic stimulation.

Adult↗
PubMed1982

Endocrinological features and endometrial morphology in climacteric women receiving hormone replacement therapy.

Prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), oestrone (E1), and oestradiol (E2) levels were determined in 204 women who were receiving hormone replacement therapy for their climacteric symptoms. The changes in these hormone levels and the endometrial morphology were studied in order to determine the effects of the replacement therapy. The women were divided into two groups: the first group of 120 women was treated with conjugated oestrogens administered cyclically, plus norethisterone acetate. The second group of 84 women received oral oestriol succinate, also administered cyclically but without additional progestogens. The oestrogen-progestogen therapy resulted in a disappearance of the climacteric symptoms and a significant decrease of FSH and LH levels. Oestriol therapy was less effective than the conjugated oestrogens as a replacement therapy. Oestriol therapy also resulted in a less remarkable decrease of gonadotrophin levels. There were no significant changes in prolactin levels in either group of women. The endometrial histology did not change significantly after either of the two hormone replacement therapies.

Climacteric↗
PubMed1982

Prolactin stimulation by intravenous labetalol is mediated inside the central nervous system.

We have previously reported that labetalol infusion increases prolactin (PRL) secretion in hypertensive patients. In an attempt to investigate the site where labetalol stimulates PRL, the drug was infused intravenously (100 mg) into healthy subjects, both under basal conditions and after pretreatment with L-dopa plus carbidopa (250 mg and 25 mg respectively every 6 h for 1 day), since this regimen has been reported to blunt the PRL responses to centrally acting stimuli. The effects of oral labetalol administration (100 and 200 mg) on PRL was also evaluated. Serum PRL concentration did not change after oral labetalol, whereas it was increased by intravenous drug administration. This effect was completely abolished by pretreatment with L-dopa plus carbidopa. These findings, though they do not demonstrate the mechanism, suggest that the hyperprolactinaemia induced by labetalol is mediated inside the blood-brain barrier.

Administration, Oral↗
PubMed1981

Effects of chronic prazosin treatment on the renin-angiotensin-aldosterone system in man.

The effects of chronic prazosin treatment (3 mg/day for three weeks) on plasma renin activity (PRA) and plasma aldosterone (PA) levels were evaluated in 12 hypertensive patients, under conditions of metabolic balance. After three weeks of drug administration no significant change occurred in PRA as well as PA levels, with respect to pretreatment values, both in basal conditions and following 2 hours of ambulation. No change was observed in heart rate, while a fall in both systolic (P less than 0.02) and diastolic (P less than 0.05) blood pressure occurred in supine as well as in deambulation-stimulating condition. A mild increase in body weight (P less than 0.05) and a decrease in serum sodium (P less than 0.05) was induced by prazosin treatment. These findings are in keeping with the pharmacologic properties of prazosin, which is a selective blocker of postsynaptic alpha adrenoreceptors and therefore lowers vascular resistance without reflex sympathetic overactivity. The moderate volume expansion after prazosin does not appear to be aldosterone mediated.

Adult↗
PubMed1981

Effect of loperamide, a peripheral opiate agonist, on circulating glucose, free fatty acids, insulin, C-peptide and pituitary hormones in healthy man.

The effect of acute oral administration of loperamide (4, 8 and 16 mg), a peripheral opiate agonist used in the treatment of diarrhoea, on several metabolic and endocrine variables has been evaluated in healthy volunteers in comparison with placebo. Plasma glucose was significantly raised by all three doses, whereas serum IRI and C-peptide were decreased and serum FFA was significantly increased only after loperamide 8 and 16 mg; serum PRL, GH, LH and FSH did not change. The data suggest that opiates may be involved in the regulation of glycaemia, probably by modifying islet hormone secretion by acting at a peripheral site, since loperamide does not cross the blood-brain barrier. Although the precise mechanism of these actions is unknown, it is suggested that the effects of loperamide are mediated either by stimulation of opiate receptors per se, or by suppression of acetylcholine release from cholinergic nerve endings. The lack of change in pituitary hormone secretion by loperamide is in agreement with previous observations indicating that opiate effects on PRL, GH and gonadotropins occur at the level of the central nervous system.

Adult↗
PubMed1981

Oral glucose tolerance and insulin response after one week's clonidine treatment in hypertensive patients.

Acute clonidine administration is known to induce a significant rise in plasma glucose in man. In order to evaluate the possible effect of prolonged drug treatment on glucose metabolism, paired OGTTs were performed in 12 hypertensive patients (6 with normal and 6 with abnormal glucose tolerance) in basal conditions and following 1-week's administration of clonidine (0.15 mg every 8 h) Basal plasma glucose and serum insulin concentration as well as glucose tolerance and insulin response to oral glucose did not change in either group after treatment. Although the mechanism(s) mediating the transient hyperglycemic action of clonidine are not fully understood, the present findings indicate that this drug does not exert diabetogenic effects during chronic treatment, and suggest that homeostatic mechanisms may counteract the acute effect of clonidine on glucose metabolism.

Adult↗
PubMed1981

Inhibition of the renin-angiotensin-aldosterone system by L-dopa with and without inhibition of extracerebral dopa decarboxylase in man.

1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man. 2. Eight normal subjects received in a randomized order placebo, L-dopa (500 mg, orally) and L-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses). 3. L-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P less than 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P less than 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P less than 0.05 at 120 and 150 min, P less than 0.01 at 180 min) and in plasma aldosterone concentration (P less than 0.05 at 30 and 60 min, P less than 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens. 4. Since L-dopa, as well as L-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.

Adult↗
PubMed1981

Serum Gastrin concentration in patients with rheumatoid arthritis: effect of long-term immunosuppressive or antidopaminergic treatment.

In an attempt to further evaluate the conflicting incidence of hypergastrinemia in patients with rheumatoid arthritis (RA), serum gastrin concentration has been determined in 58 RA patients and in 58 healthy subjects. Mean levels were significantly higher in RA patients than in controls, although clearly high values were only found in 3 subjects with severe hypochloridria. During one year of immunosuppressive treatment in 12 RA patients with cyclophosphamide plus colchicine serum gastrin levels did not change, while a significant decrease was observed in another 12 patients after 2 months' treatment with haloperidol, a dopamine receptor blocker; this decrease was sustained throughout the one year treatment. Indomethacin administration up to 6 months did not change serum levels in a control group of 12 RA patients. Serum gastrin concentration in patients treated with haloperidol was significantly lower than in those treated with indomethacin at 2 and 6 months, while no significant differences were observed between cyclophosphamide- and indomethacin-treated groups. These results confirm and extend previous studies showing inhibition of gastrin secretion by antidopaminergic drugs. No correlations were observed between serum gastrin levels and inflammatory indices, both in basal conditions and during any drug treatment.

Adult↗
PubMed1981

Effect of loperamide and naloxone on gastric acid secretion in healthy man.

The effect of acute oral administration of three different doses (4, 8, and 16 mg) of loperamide, a peripheral opiate agonist, on basal and submaximal pentagastrin-stimulated gastric acid secretion was evaluated in healthy volunteers. Both basal and stimulated gastric secretion were significantly lowered by 8 and 16 mg of the drug in comparison with a control study, while 4 mg was ineffective. Naloxone, a specific opiate antagonist, decreased slightly but not significantly both basal and pentagastrin-stimulated gastric acid secretion, when infused intravenously at the rate of 30 micrograms/kg/h, but completely abolished the inhibitory effect of loperamide on gastric acidity. These data also suggest that opiates may be involved in the regulation of gastric acid secretion in man by acting at a peripheral site, as loperamide does not cross the blood-brain barrier.

Adult↗
PubMed1981

Central nervous system and pituitary mechanisms in dopaminergic stimulation of growth hormone release in women.

In an attempt to evaluate the relative importance of brain and peripheral (i.e., outside the blood-brain barrier) dopamine (DA) receptor stimulation in the regulation of GH release, DA (5 microgram/kg/min infused i.v. for 120 min), L-dopa (500 mg p.o.), L-dopa (100 mg p.o.) plus carbidopa (35 mg p.o.) after pretreatment with carbidopa (50 mg p.o. every 6 h for 1 day), and nomifensine (200 mg p.o.) have been administered to healthy women. Significant elevations in serum GH were induced by all regimens in comparison with a control placebo study, although the effect of DA was only transient in spite of continuing infusion. The between drugs analysis revealed that L-dopa alone was significantly more effective in releasing GH than carbidopa plus L-dopa as well as DA infusion and nomifensine administration. These results suggest that both central nervous system and peripheral mechanisms are involved in dopaminergic stimulation of GH release in man. Since DA does not affect somatotropes directly, increased serum GH levels by DA infusion probably reflect stimulation of median eminence dopaminergic neurons.

Adolescent↗
PubMed1981

Inhibition of luteinizing hormone release by dopamine infusion in healthy women and in various pathophysiological conditions.

To investigate the effect of dopaminergic stimulation on gonadotrophin release, serum LH and FSH concentrations were measured during dopamine infusion (5 microgram/kg/min for 120 min) in 8 healthy women in the early follicular phase, in 12 patients with hyperprolactinaemic amenorrhoea, in 5 subjects with premature ovarian failure and in 8 with polycystic ovarian disease and raised serum LH levels. Dopamine infusion produced a significant LH decrease compared with a control study using saline in all groups; there were no significant changes in FSH concentration. Between groups analysis showed a significantly greater LH fall in patients with polycystic ovarian disease than in the other groups. Dopamine inhibits LH release in healthy women and patients with anovulatory states of varying aetiology, and enhanced sensitivity to this inhibitory mechanism exists in polycystic ovarian disease. This finding suggests reduced dopamine activity at the median eminence level in this condition.

Adolescent↗
PubMed1980

[Ileo-ceco-colic invagination. Apropos of a case caused by lymphoma of the last ileal loop].

An unusual case of intestinal invagination due to lymphoma of the last ileal segment serves as a basis for a review of the pathogenetic mechanisms underlying the invagination process and its different onset modalities. Special attention is paid to how chronic invaginations, as a result of their varied, unremarkable symptomatology, often involve mistaken or late diagnosis. The present case is noteworthy because of the summing of factors proper to primary invagination with those of secondary invagination. The hyperperistaltism resulting from the presence of a non-pedunculated mass acted on an intestinal segment in which the anatomico-functional conditions for the establishment of primary invagination were often present., All this was responsible for a chronic basic ileo-caecal invagination process, the cause of progressive limming with acute episodes of further advance of the invaginated part to the transverse colon. It was these acute episodes that gave clinical dignity to the insidious symptomatology reported by the patient thus allowing speedy, correct diagnosis of the ongoing neoplastic process and hence radical surgery with favourable prognosis.

Adolescent↗
PubMed1980

Effect of two antiserotoninergic drugs, methysergide and metergoline, on gastric acid secretion and gastrin release in healthy man.

The effects of acute oral administration of the antiserotoninergic drugs methysergide (3 mg) and metergoline (4 mg) on basal, submaximal (0.6 micrograms/kg i. m.) and maximal (6 micrograms/kg) pentagastrin-stimulated gastric acid secretion, as well as on basal and food-induced gastrin release, have been evaluated in healthy volunteers. Methysergide significantly increased basal and submaximal pentagastrin-stimulated gastric acid secretion, and metergoline significantly inhibited gastric acidity in all experiments. Basal and stimulated serum gastrin concentrations were not modified by either drug. The effect of methysergide on gastric acid secretion was opposed to that of serotonin and was probably dependent on its antiserotoninergic action, but the decrease in gastric acidity caused by metergoline is not easily explained. Although the effect is similar to that of a dopamine infusion, it does not depend on dopamine infusion, it does not depend on dopamine receptor stimulation, since it was not influenced by pretreatment with metoclopramide. It is suggested that it might be due to the weak anticholinergic and/or antihistaminic properties of metergoline.

Adult↗