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Biomedical subjects

R Caldara

Publications and source records attributed to R Caldara.

At least 91 records · Page 5Linked to original sources
PubMed1980

Gastric acid and gastrin secretion after administration of the anti-inflammatory drug, sulindac, in man.

The effects of oral administration of the anti-inflammatory drug, (Z)-5-fluoro-2-methyl-1-[p-(methylsulfinyl)-benzylidene]-indene-3-acetic acid (sulindac, Clinoril) 400 mg/d for 8 days, on basal and submaximal (3 micrograms/kg b.2. i.m.) and maximal (6 micrograms/kg b.w.) pentagastrin-stimulated gastric acid secretion as well as on serum gastrin concentration have been evaluated in female patients affected with osteoarthrosis. No significant changes in either gastric acid or gastrin secretion were induced by the treatment. Serum gastrin levels were also unaltered after acute administration of 200 mg sulindac. These results confirm and extend previous observations suggesting that the drug does not exert major actions on the stomach.

Adult↗
PubMed1980

Clonidine-induced hyperglycemia: evidence against a growth hormone-mediated effect.

The effects of acute clonidine infusion (0.15 mg over 10 min) on several endocrine and metabolic variables have been evaluated in 12 hypertensive patients and 12 normotensive controls. Plasma glucose increased significantly in comparison with a placebo study in both groups; serum growth hormone showed a significant increase in healthy subjects but did not rise in hypertensive patients; there was no correlation between the increments in plasma glucose and in serum growth hormone in the whole group of subjects; serum-free fatty acids, insulin, prolactin and plasma cortisol did not change in any group. These data, although not excluding a central site of the clonidine hyperglycemic action, contrast the view that it may depend on stimulation of growth hormone release.

Adult↗
PubMed1979

Improved oral glucose tolerance following antiserotonin treatment in patients with chemical diabetes.

The effects of short-term treatment with either placebo or two serotonin antagonists, cyproheptadine and metergoline, on oral glucose tolerance and insulin secretion have been evaluated in normal subjects and in patients with chemical diabetes. Placebo treatment was not associated with any significant change in the parameters examined. Glucose tolerance in chemical diabetics was significantly improved both after cyproheptadine and metergoline; fasting plasma glucose was also reduced by metergoline. Treatment with the latter drug was also associated with a significant decrease in incremental glucose area in healthy subjects, which was not affected by cyproheptadine. Basal and glucose-stimulated insulin secretion were not affected by either drug in any subjects. Cyproheptadine and metergoline improve glucose metabolism in chemical diabetes probably by reducing insulin resistance. This may depend either on decreased secretion of counter-regulatory hormones or on a direct pharmacological action of the drugs on glucose utilization, possibly mediated by their common antiserotoninergic properties.

Adult↗
PubMed1979

Prolactin release by intravenous cimetidine in man: evidence for a suprapituitary locus on action.

In an attempt to identify the sites at which cimetidine stimulates prolactin release, the drug was administered intravenously (6 mg/kg body weight) to healthy subjects under basal conditions, during dopamine infusion (1 microgram/Kg-min for 120 min) and after pretreatment with L-dopa plus carbidopa (250 plus 25 mg every 6 for 1 day). The serum prolactin response to cimetidine was abolished by dopamine infusion and almost completely suppressed by L-dopa plus carbidopa administration. These findings suggest that the drug acts on the central nervous system to stimulate prolactin release. Although the mechanism of this action is unclear, it does not seem to depend on an antidopaminergic effect and may be related to blackade of brain H2 histamine receptors.

Adult↗
PubMed1978

Restoration of cyclic ovarian function by metergoline treatment in a patient with a prolactin-secreting pituitary microadenoma.

A patient with amenorrhea due to a prolactin-secreting pituitary microadenoma was treated with the antiserotoninergic drug metergoline for 8 months. The first menstruation occurred after 1 month of therapy, and it was followed by regular menses by the 3rd month. Presumptive evidence of ovulation was obtained in at least some instances by serum progesterone and gonadotropin determination. Serum prolactin was only slightly lowered by treatment. The patient had menses and possibly ovulation in the 2 months following drug withdrawal. Metergoline might restore ovarian function in hyperprolactinemic amenorrhea either by prolactin suppression or perhaps by direct stimulation of gonadotropin release.

Adenoma↗
PubMed1978

Inhibition of prolactin release by serotonin antagonists in hyperprolactinemic subjects.

Metergoline (4 mg) and methysergide (3 mg), two serotonin antagonists known to inhibit prolactin secretion in normal subjects, and the dopaminergic agonist, bromocriptine (2.5 mg) were orally administered in hyperprolactinemic patients. Mean serum prolactin concentration was significantly decreased between 120 and 240 min following the ingestion of all three drugs in comparison with a placebo; a consistent reduction to below 50% of basal values occurred in 10 of 14 patients after metergoline, in 5 of 10 after methysergide, and in 11 of 14 after bromocriptine administration. These data indicate that serotonin antagonists may acutely lower serum prolactin levels in hyperprolactinemic patients similarly to bromocriptine, though their mechanism of action is most likely different.

Adult↗
PubMed1978

Increased glucose disappearance rate after short-term clofibrate administration in normal subjects and in patients with chemical diabetes.

Following seven days clofibrate administration, the glucose disappearance rate during an intravenous glucose tolerance test was significantly increased in 6 normal subjects and in 11 patients with chemical diabetes. Both the acute and the total insulin secretory response were unchanged. Though fasting serum levels of free fatty acids, triglycerides, and cholesterol were significantly lowered by treatment, no correlation was found between the decrease in serum lipids and the increase in glucose disappearance rate. It is suggested and clofibrate improves glucose utilization by reducing insulin resistance irrespective of its effects on serum lipids concentration.

Blood Glucose↗
PubMed1978

Effect of dopamine infusion on gastric and pancreatic secretion and on gastrin release in man.

The effect of dopamine infusion on basal and pentagastrin-stimulated gastric secretion, on basal and secretin-CCK-PZ-stimulated pancreatic secretion, and on basal and meal-induced gastrin release has been evaluated in healthy volunteers. Both basal and stimulated gastric acid secretion were significantly inhibited during dopamine infusion with a significant rebound to pre-infusion values after discontinuing dopamine. These effects were prevented by pretreatment with the antidopaminergic drug, metoclopramide. A slight but now significant decrease in amylase and bicarbonate outputs was also observed during dopamine infusion, while gastrin release did not change. These data suggest the existence of dopaminergic mechanisms in the regulation of gastric acid secretion in man.

Adult↗
PubMed1978

Prolactin suppression by serotonin antagonists in man: further evidence for serotoninergic control of prolactin secretion.

To further investigate the role of serotonin in human prolactin (Prl) secretion, serotonin antagonists have been administered to healthy volunteers in basal conditions and after pretreatment with the selective blocker of dopamine receptors, pimozide (Pim). Highly significant falls (p less than 0.001) in serum Prl were observed at 120, 180, and 240 min following the oral administration of metergoline (Met) (4 mg; N = 34) and methysergide (Meth) (3 mg; N = 20) in comparison with placebo. No significant difference was found in the degree of Prl suppression induced by these two serotonin antagonists and by hte dopaminergic drug bromocriptine (Br) (2.5 mg; N = 20). After Pim pretreatment (1 mg every 6 h for 7 days) the elevated serum Prl levels were reduced to 27.1% +/- 8.1 (SEM) of basal after Met and to 54.5% +/- 8.9 after Meth administration (N = 5 for each study). It is concluded that Met and Meth inhibit Prl secretion by mechanisms which are not or only partially related to dopaminergic receptors. These data are consistent with a stimulatory role for serotonin in human Prl release.

Adolescent↗
PubMed1978

Inhibition of gastrin secretion by sulpiride treatment in duodenal ulcer patients.

The serum gastrin response to whole beef extract was measured in 14 duodenal ulcer patients before and after sulpiride administration. A significant inhibition of response was found both after acute intramuscular injection of the drug and after oral administration for 1 week. Fasting serum gastrin was also significantly reduced after chronic treatment; gastric acid secretion did not change. Although the mechanism of the gastrin-lowering action of sulpiride is unknown, it could be mediated by some known effects(s) of the drug, such as modifications in brain monoamine metabolism or perhaps reduced growth hormone secretion.

Administration, Oral↗
PubMed1978

Failure of lysine-acetylsalicylate and phenylbutazone to affect gastrin secretion in healthy adults.

The effect of acute parenteral and chronic oral administration of lysine-acetylsalicylate and phenylbutazone on fasting and meal-stimulated serum gastrin levels was investigated in healthy volunteers. No significant changes in gastrin secretion were induced by any treatment. The results confirm and extend previous observations suggesting that the ulcerogenic properties of salicylates and phenylbutazone are not related to increased gastrin secretion.

Administration, Oral↗
PubMedDate not supplied

Effect of bromocriptine administration on gastric acid and gastrin secretion in man.

The effects of acute oral administration of the dopaminergic drug, bromocriptin (5 mg), on basal and submaximal (1 and 3 microgram per kg bw given sc) and maximal (6 mug per kg bw) pentagastrin-stimulated gastric acid secretion and on basal and meal-induced gastrin release have been evaluated in healthy volunteers. Although basal and maximal pentagastrin-stimulated acid output did not change, the response to submaximal pentagastrin doses was significantly increased. Basal and stimulated serum gastrin concentrations were not modified, nor was fasting serum gastrin during chronic bromocriptine treatment (10 mg per day for 90 days) in acromegalic patients. As dopamine infusion is known to reduce basal and pentagastrin-induced gastric acid secretion, the presently reported effect of bromocriptine is not dependent on dopamine receptor stimulation. It is suggested that it might be due to alpha-adrenergic and/or serotoninergic antagonism, both actions being properties of bromocriptine. Alternatively, since bromocriptine, at variance with iv infused dopamine, crosses the blood-brain barrier, the effect of this drug on gastric function might depend on interference by centrally mediated actions on those directly exerted at the gastric level.

Acromegaly↗
PubMedDate not supplied

Stimulation of prolactin release by intravenous cimetidine: a dose-response study.

The PRL response to iv cimetidine was tested in 8 healthy males and 8 females at 4 different dose levels (0.75, 1.5, 3.0 and 6.0 mg/kg bw). Serum PRL levels were significantly increased in comparison with a placebo study by the second cimetidine dose in both sexes. The PRL response was significantly higher in females than in males at all but the lowest dose tested. A significant correlation between the cimetidine dose and the PRL response was observed. There was no significant modifications in serum GH, LH, FSH, IRI and glucose. Present findings demonstrate that the stimulation of PRL release by iv cimetidine is quite specific and dose-dependent.

Adult↗