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Results for “Prolactin Release-Inhibiting Factors”

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PubMed1976

Suppression of postpartum lactation with furosemide.

A regimen of fursemide and moderate restriction of fluid intake was followed in 120 postpartum women to suppress lactation. The methods and results are presented, and possible mechanisms whereby furosemide may suppress lactation are discussed.

Depression, Chemical↗
PubMed1979

[Clinical importance of antiprolactinaemic treatment of functional infertility (author's transl)].

Reported in this paper is the effectiveness of antiprolactinaemic treatment of 40 infertile women. All case histories revealed previous unsuccessful attempts to induce ovulation. Antiprolactinaemic treatment was in all cases preced by RIA determination of prolactin and gonadotrophin. Prolactin levels were found to be somewhat increase in 19 cases, while 21 women were normal. The gonadotrophin plasma levels usually were closer to the lower limits of normal values. The presence of hypophyseal adenoma had been ruled out beforehand. Long-time treatment was based on the administration of 5 mg Parlodel/die. The effect was excellent in all cases of hyperprolactinaemia, but response was recorded, as well, from a group of patients with normal prolactin levels. Galactorrhoea ceased to exist in all cases. Clomiphen was applied again to induce ovulation in those patients who had not responded at all or developed only bleeding without ovulation. That treatment proved to be effective in several cases.

Adult↗
PubMed1975

Effect of ergoline derivative VUFB-6638 on the adenohypophysial prolactin concentration in rats.

The compound VUFB-6638 (N-/D-6-methyl-8-isoergolin-I-yl/N'-N'-diethylurea hydrogen maleinate) was administered for four consecutive days to lactating rats in daily oral doses of 0.1, 1.0 and 2.0 mg/kg. The adenohypophysial prolactin concentration decreased by 34% to 68%, respectively. Moreover, this compound reduced or even completely suppressed the lactation. In view of the assumed relations between prolactin and breast carcinoma, a potential use of the drug is noted.

Animals↗
PubMed1979

Failure of MIF-I to affect behavioral responses in patients with Parkinson's diseases under L-dopa therapy.

In eight subjects with Parkinson's disease under an optimal daily dose of L-dopa, acute administration of MIF-I (200 mg i.v.) did not ameliorate either the total disability score or the intellectual test PM 38 when evaluated in comparison with the effect induced by acute administration of a placebo. Also concomitant evaluation of the effect of MIF-I on the secretion of anterior pituitary hormones which are under dopaminergic control i.e., growth hormone and prolactin, did not reveal any potentiation of the L-dopa-induced stimulus.

Aged↗
PubMed1976

Recently discovered hypothalamic-pituitary hormones.

In recent years a variety of peptide hormones have been isolated from the mammalian hypothalamus and pituitary. Several hypothalamic hormones, including thyroliberin (thyrotropin-releasing factory), luliberin (luteinizing hormone-releasing factor), and somatostatin (somatotropin release-inhibiting factor), have been characterized and synthesized. The subsequent development of radioimmunoassays for these hormones has made possible the study of their physiology. The measurement of prolactin in serum and the release of pituitary hormones after the administration of the hypothalamic hormones has proved to be useful in clinical diagnosis. The use of hypothalamic hormones in treating various clinical disorders and the isolation and characterization of new releasing and inhibiting hormones in the hypothalamus are actively being investigated.

Acromegaly↗
PubMed1976

Effects of thyrotropin-releasing hormone on prolactin, growth hormone and corticosterone secretions in adult male rats treated with pentobarbital or morphine.

Thyrotropin-releasing hormone (TRH) injected either IP (10 mg/kg) or intraventricularly (10 mug/rat) antagonized the pentobarbital-induced secretion of prolactin (PRL). This effect was not blocked by propranolol. In thyroidectomized animals the effect was not apparent; tri-iodothyronine (T3) injection was however ineffective. The injections of luteinizing hormone-releasing hormone (LH-RH) and of melanocyte stimulating hormone release-inhibiting factor (MIF) were also ineffective. Of six TRH analogues, only those containing histidine antagonized pentobarbital-induced PRL release, but none modified plasma levels of growth hormone (GH) or corticosterone (B). Brain levels of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were not modified by TRH. Morphine-induced secretion of PRL and GH was also significantly antagonized by TRH. Since pentobarbital and morphine-induced hormonal changes are probably exerted through a central nervous system depressant action, these data indicate that TRH can influence brain activity through an extrapituitary mechanism.

Animals↗