Growth hormone and prolactin secretion in liver cirrhosis: evidence for dopaminergic dysfunction.
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Biomedical subjects
Publications and source records attributed to C Barbieri.
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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.
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.
The effects of oral administration of 2 mg prazosin on several metabolic and endocrine variables were evaluated in 12 patients with hypertension (6 with normal and 6 with abnormal glucose tolerance). Prazosin was followed by a rise in plasma glucose and serum free fatty acids (FFA) in both normal and diabetic subjects; there was a trend upward in serum albumin (IRI), but growth hormone (GH), prolactin (PRL), and gastrin did not change. Although these results are in general agreement with metabolic effects of other alpha adrenergic blockers already reported, the rise in plasma glucose is at variance with studies performed with phentolamine.
1. In an attempt to test the hypothesis of a derangement in central catecholaminergic function in hypertensive patients, the serum growth hormone and prolactin responses to the alpha-adrenergic agonist clonidine (0.15 mg infused intravenously) and to L-dopa administration (500 mg orally) were evaluated in 15 hypertensive and 15 normotensive subjects matched for sex, age and body weight. 2. Whereas L-dopa elicited a growth hormone response of similar magnitude in both groups, clonidine infusion induced a significant increase in serum growth hormone in normotensive, but not in hypertensive, subjects. 3. Prolactin levels were equally suppressed by L-dopa and did not change after clonidine in either group. 4. The present study adds neuroendocrine evidence to the concept of a derangement in central alpha-adrenergic function in human hypertension.
The effects of chronic (3 mg/day for 1 week) administration of the vasodilator drug prazosin on several metabolic and endocrine variables were evaluated in 12 hypertensive patients, 6 with normal and 6 with abnormal oral glucose tolerance test (OGTT). After 1 week prazosin treatment there were no significant modifications in fasting plasma glucose, serum free fatty acids (FFA), cholesterol, triglycerides, insulin (IRI), growth hormone (GH), prolactin (PRL) and gastrin levels; oral glucose tolerance and IRI response to glucose were unchanged in normal subjects, while in chemical diabetics there was a significant improvement in glucose tolerance and a slight increse in IRI secretion. Therefore, the untoward metabolic effects of acute prazosin administration, i.e. increased plasma glucose and serum FFA, are not sustained during chronic treatment, which may even improve glucose metabolism in diabetic patients.
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The effect of 1 week of oral treatment with four antidopaminergic drugs--metoclopramide, sulpiride, haloperidol, and pimozide--on fasting and meal-stimulated serum gastrin levels has been evaluated in healthy subjects. All of the four drugs significantly reduced the gastrin response to a meal, whereas basal concentration was unaffected. It is suggested that this action is mediated by central nervous system dopamine receptor blockade, which might act either via nervous or humoral mechanisms to inhibit gastrin release.
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.
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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.
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.
Fructose-1,6-diphosphate (FDP) is able to abolish oxytocin induced spastic inertia in rat uterus. The clinical use of FDP is suggested by observation carried out on 30 deliveries with oxytocin induction. The FDP-treated patients (5 g of FDP in 50 ml of water by intravenous infusion) showed a statistically significant decrease of time elapsed between the beginning of uterine inertia and the recovery of uterine contractions (176 +/- 25.4 min) compared to controls (562 +/- 32.5 min).
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