Effect of bromocriptin on the endocrine system and fetal development.
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Biomedical subjects
Publications and source records attributed to I Lancranjan.
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The mechanism inducing milk secretion in 10 puerperal women and in their children (Witch's milk) was studied by means of sequential hormone measurements starting at delivery and continued during the first postpartum week. Determinations included prolactin (PRL), growth hormone (GH), estradiol 17beta (E217beta), and progesterone (PG). Hormonal levels in the newborns closely paralleled those of the mothers. In both groups, the onset of milk secretion coincided with the disappearance of sex steroids from plasma in the presence of elevated PRL concentrations. Response to TRH (8 microng/kg) revealed adequate PRL reserve, and failure of this peptide to modify basal GH in the neonates was suggestive of appropriate hypothalamic control. The role of estrogens in the induction of pituitary hyperplasia during pregnancy is discussed.
The effect of a new soluble ester of 1-5 hydroxytryptophan (1-5 HTP, Ro 3-5940, 200 mg infusion) on prolactin (PRL) and growth hormone (GH) release was tested in 11 young, healthy subjects (6 men, 5 women). To minimize side-effects, peripheral decarboxylase inhibition was achieved with benserazide (Ro 4-4602.) PRL increased significantly (P less than 0.01) after benserazide alone in all subjects. A further significant increase (P less than 0.01) of PRL plasma levels occurred only in women up to 90 min after the infusion of 1-5 HTP was discontinued. Benserazide administration had no effect of basal GH levels, but a significant increase of GH release (P less than 0.01) was noticed 30-120 min after the end of 1-5 HTP infusion in both men and women. The mean peak value of GH plasma levels after 1-5 HTP administration was 32.0 +/- 8.8 ng/ml. It was postulated that benserazide penetrated at the level of the pituitary, decreasing the synthesis of dopamine and consequently reducing its known inhibitory effect on PRL release. The PRL increase (statistically significant only in women), as well as the release of GH after 1-5 HTP infusion, was considered as further evidence for stimulatory serotoninergic control of both PRL and GH secretion.
Five volunteers with normal ovarian cycles received oral doses of 2 X 2.5 mg or 3 X 2.5 mg bromocriptin (CB 154)/day respectively. The treatment started at the onset of menstruation and lasted on complete cycle. In addition to the decrease of prolactin secretion, a reduction of plasma progesterone concentrations during the corpus luteum phase was demonstrated. This fall of progesterone seemed to be preferentially due to bromocriptin-induced hypoprolactinaemia and not to direct ovarian effects of the drug.
The reproductive ability of 150 men occupationally exposed to lead were studied by clinical and toxicological analysis. Subjects were divided into four groups: lead-poisoned workmen (23) and those showing a moderate (42), slight (35), or physiologic absorption (50). Findings show that (1) Lead poisoning as well as moderate increased absorption of lead decrease the fertile ability of men. An increased frequency of asthenospermia, hypospermia, and teratospermia have objectified the decrease. (2) Slight increased or physiologic absorption of lead do not significantly influence the fertile ability of workmen. (3) Hypofertility induced by lead is due, perhaps, to its direct toxic effect on the gonads, as no interference with the hypothalamopituitary axis were evidenced.
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The incidence of chromosome aberrations was studied by peripheral blood incubation (52 hr, the last 4 hr in the presence of Colcemid) using a modification of the Evans' technique in twenty-two men exposed to either vapors of metallic mercury (Group I) or organic mercury (Group II). Mercury concentrations of the work areas frequently exceeded the Maximum Allowable Concentrations in the past. During the year proceding the investigation, mercury values ranged between 0.15 and 0.44 mg/m3. None of the investigated men were poisoned, but all had had repeated increased mercury absorption with urinary eliminations reaching 890 microgram/l and 896 microgram/l for subjects in Groups I and II, respectively. The incidence of chromosome aberrations was significantly higher (P less than .001) in subjects exposed to mercury as compared with a control group (ten subjects) of a similar mean age. There was no statistical difference in the incidence of chromosome aberrations between men belonging to Groups I and II. Although an increase of both chromatid gaps and breaks was noticed in exposed men, the incidence did not significantly differ from controls. No chromatid interchanges were recorded and no difference between exposed and control subjects was noticed concerning the frequency of aneuploid or polyploid cells.