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Biomedical subjects

G Delitala

Publications and source records attributed to G Delitala.

At least 127 records · Page 7Linked to original sources
PubMed1977

Action of metergoline in suppressing prolactin release induced by mechanical breast emptying.

Ten women were studied during the first post-partum week. Mechanical breast emptying with a breast pump for 30 min induced a marked increase in plasma prolactin (PRL) reaching a maximum 30 min after the beginning of stimulation. In all patients oral administration of the antiserotonin agent metergoline, 8 mg daily for two days, completely blocked any PRL secretion induced by breast stimulation. These results confirm the inhibitory effect of metergoline on PRL release.

Adult↗
PubMed1977

Suppression of thyrotropin (TSH) and prolactin (PRL) release by pyridoxine in chronic primary hypothyroidism.

A single iv dose of pyridoxine (V) (300 mg) caused a significant decrease in the concentration of serum thyrotropin (TSH) in 6 patients with primary hypothyroidism. There was no consistent change in serum thyroxine and triiodothyronine concentrations suring the experiment. The serum prolactin (PRL) levels were also suppressed by pyridoxine administration. These findings suggest that pyridoxine inhibits TSH secretion as well PRL by a direct action on the hypothalamus or pituitary gland.

Adult↗
PubMed1977

Stimulating action of sulpiride and pimozide on prolactin release. Effect on bromocriptine, L-dopa and metergoline administration.

In order to evaluate the mechanism of action of metergoline, an antiserotonin agent, the effect of pre-treatment with metergoline on prolactin (PRL) release induced by sulpiride was compared to that obtained after bromocriptine administration in normal subjects. In addition, the metergoline effect on PRL release induced by pimozide, specific dopamine receptor blocking agent, was compared to that obtained with L-dopa. Metergoline administration resulted in definite decrease in plasma PRL in all subjects; however, metergoline did not block, differently from bromocriptine, the PRL release induced by sulpiride. On the contrary, metergoline, like L-dopa, inhibited PRL release induced by pimozide pre-treatment. These results raise the possibility that metergoline does not act as an antiserotonin agent; its antilactogenic effect observed under basal conditions may be dependent on different mechanisms of action.

Adolescent↗
PubMed1977

Dissociation of growth hormone and prolactin response to levodopa during pyridoxine administration.

500 mg of levodopa was administered orally to 8 normal subjects and induced an increase of growth hormone (GH) and a decrease of prolactin (PRL) secretion. The levodopa-induced GH release was inhibited by an intravenous infusion of pyridoxine; on the contrary, the PRL response to levodopa was enhanced by pyridoxine infusion. This dissociation of GH and PRL responses to levodopa during pyridoxine infusion appears to be mediated by peripheral acceleration of the conversion of levodopa to dopamine. Since dopamine does not penetrate the blood-brain barrier, the enhanced PRL decrease observed during pyridoxine infusion might be explained only on the basis of a mechanism of action exerted by dopamine on extra blood-brain barrier sites.

Adult↗
PubMed1977

Suppression of pimozide-induced prolactin secretion by piridoxine (vitamin B6).

I.V. administration of 300 mg. Pyridoxine caused an acute fall in prolactin (PRL) plasma levels in six normal subjects. Like levodopa, pyridoxine suppressed the increase in PRL secretion induced by treatment with pimozide, a specific dopamine receptor blocking agent. These findings further support the hypothesis that vitamin B6 stimulates dopaminergic activity at hypothalamic and/or hypophyseal level.

Adult↗
PubMed1976

Effect of metroclopramide on serum prolactin levels in humans.

The effect of acute and chronic administration of metoclopramide on serum prolactin levels in normal subjects was studied. Metoclopramide 10 mg i.v. induced a prompt rise in serum prolactin levels in all subjects. At 180 min the levels remained high. Prolactin levels were markedly elevated during a 5 day course of treatment with metoclopramide in six subjects. It is suggested that metoclopramide could be used in the functional exploration of the hypothalamic-pituitary axis.

Adult↗
PubMed1976

Effect of pyridoxine on human hypophyseal trophic hormone release: a possible stimulation of hypothalamic dopaminergic pathway.

A single dose of pyridoxine (300 mg iv) produced significant rises in peak levels of immunoreactive growth hormone GH and significant decrease of plasma prolactin PRL in 8 hospitalized healthy subjects. Serum glucose, luteinizing hormone LH, follicle stimulating hormone FSH and thyrotropin TSH were not altered significantly. In addition, in 5 acromegalic patients who were studied with both L-dopa and pyridoxine, inhibition of GH secretion followed either agent in a similar pattern. These data suggest a hypothalamic dopaminergic effect of pyridoxine.

Acromegaly↗
PubMed1976

Growth hormone and prolactin release in acromegalic patients following metergoline administration.

In six acromegalite patients oral administration of 4 mg of metergoline, an antiserotonin agent, produced a fall in plasma growth hormone (GH) and prolactin (PRL) concentrations. In the same patients this inhibitory effect was observed after administration of dopaminergic drugs, L-Dopa and 2-Br-alpha-ergocryptine. Both GH and PRL levels remained suppressed during a 6 day course of treatmnt with metergoline. These results are consistent with the hypothesis that the inhibitory effect of netergoline on GH and PRL release is determined by inactivation of serotonin receptors in the hypothalamus or at the pituitary.

Acromegaly↗
PubMed1976

Plasma prolactin response to L-dopa TRH and metaclopramide in thyrotoxicosis.

The plasma PRL repsonse to synthetic TRH, L-dopa and metaclopramide was evaluated in patients with thyrotoxicosis. A PRL response similar to thtaclopramide,while no PRL response was observed after TRH. When the TRH-test was repeated after treatment, all patients showed a normal increment in plasma PRL. This data suggests that, in thyrotoxicosis, PRl response to TRH only is impaired, but PRL can be suppressed by L-dopa or released by metaclopramide notwithstanding the elevated values of thyroid hormone levels.

Female↗