Cimetidine effects on prolactin release and production.

The effect of cimetidine 1600 mg. daily for three months on prolactin and related hormones is reported. Basal prolactin levels rose slightly but not significantly. There was no change in basal thyroid and sex hormone levels nor in the prolactin, gonadotrophin or thyrotrophin responses to releasing hormone stimulation. Since intravenous cimetidine induces a transient hyperprolactinemia it appears that cimetidine may facilitate release of prolactin but has no effect on its synthesis.     

Cimetidine and plasma levels of gonadotropins,prolactin and gonadal steroids in women.

The endocrine effects of cimetidine (Tagamet) during the menstrual cycle were investigated in seven healthy female volunteers. The subjects were studied for six menstrual cycles divided into the pretreatment phase, a phase of therapy with 1.2 g of orally administered cimetidine daily for two cycles, and a post-treatment phase. Cimetidine therapy induced a significant increase in the mean plasma level of follicle-stimulating hormone during the periovulatory period, followed by modest but sustained hyperprolactinemia throughout the luteal phase of each cycle. No significant changes were found in the mean plasma levels of luteinizing hormone and progesterone, and the mean plasma estradiol level was significantly decreased only in the midproliferative phase of each cycle. The mean plasma prolactin levels after a bolus injection of thyrotropin-releasing hormone in the midluteal phase during cimetidine administration did not differ from the mean control levels, which indicates that cimetidine modulates the release of prolactin at the suprapituitary locus. However, the significance of the endocrine changes remains to be established.     

Tetrahydrocannabinols and serum prolactin levels in man

δ⁹-THC, 11-OH-δ⁹-THC or placebo was administered to casual marihuana smokers in a double-blind, crossover study. δ⁹-THC and 11-OH-δ⁹-THC produced marked pharmacologic and psychologic effects (tachycardia, increased symptom score and psychologic high). In contrast to effects produced by many other centrally acting drugs, the acute administration of these cannabinoids was devoid of any significant effect on prolactin secretion as determined by monitoring changes in serum prolactin levels.     

Cimetidine and hyperprolactinemia

Plasma TSH was determined in 12 normal subjects before and after administration of mg 400 of cimetidine i.v., an H2-receptor antagonist. TSH concentration remained unchanged. In 7 normal subjects, pretreated with bromocriptine; variation of plasma prolactin were studied before and after administration of mg 400 and 800 of cimetidine. Bromocriptine inhibited the increase of prolactin secretion, induced by cimetidine. It can be assumed that: a) cimetidine doesn't release hypothalamic TRH in portal vessels; b) that drug has no direct effect on pituitary cells; c) hypothalamic H2-receptor blockade by cimetidine decreases dopamine release from hypothalamus to pituitary gland.     

Raised serum prolactin levels in amenorrhoea.

Serum prolactin levels measured by specific radio-immunoassay were over 30 mug/l in seven out of 25 women with amenorrhoea and in eight women with the amenorrhoe-galactorrhoea syndrome. There was no apparent relationship between these levels and levels of follicle-stimulating hormone, luteinizing hormones, and thyroid-stimulating hormone. Bromocriptine caused a transient fall in the proclatin levels in six out of seven cases, and in three menstruation and ovulation were restored. Estimation of serum prolactin may become important in assessing the degree of hypothalamic-pituitary dysfunction in amenorrhoea, and it may help in identifying a subgroup of patients at risk of developing a pituitary tumour or patients who may respond to specific treatment.     

Clozapine increases rat serum prolactin levels.

Clozapine differs from other anti-psychotic drugs in that is produces little or no extrapyramidal side effects. The effects of clozapine on rat brain dopamine differ markedly from those of the neuroleptic drugs. The neuroleptics increase rat serum prolactin levels which has been attributed to their dopamine receptor blocking properties. We found that clozapine markedly increased serum prolactin levels in male rats when injected intraperitoneally in doses of 5, 10, 50 and 100 mg/kg. Serum prolactin levels after 5 mg/kg clozapine were significantly less than in rats given 10, 50 and 100 mg/kg which did not significantly differ from each other. Serum prolactin after 10 mg/kg clozapine was significantly greater than after chlorpromazine, 5 mg/kg and haloperidol, 0.5 mg/kg. The increases in serum prolactin are attributed to clozapine's ability to produce dopamine blockade or to inhibit nerve impulse-dopamine release, or both. The capacity of clozapine to affect brain serotonin and norepinephrine metabolism and its strong anti-cholinergic properties are probably not involved in its ability to increase serum prolactin.     

Measurement of serum prolactin and the effect of ketamine anesthesia on serum prolactin levels in cynomolgus monkeys (Macaca fascicularis)

The effect of an anesthetic, ketamine, on the serum prolactin level was examined in wild-originating female cynomolgus monkeys (Macaca fascicularis) imported from South East Asia. Serum prolactin levels were measured by the homologous radioimmunoassay system which was developed for human prolactin. The validity was confirmed by using an extract of pituitary gland from a female cynomolgus monkey as well as serum and amniotic fluid from a pregnant monkey. Additionally, serum luteinizing hormone (LH) levels were determined by the radioreceptor assay system developed in our laboratory using Leydig cells collected from rat's testes as a receptor fraction. The experiment was repeated three times at one-month interval, using twenty animals that were divided into three groups consisting of 5, 7 and 8 monkeys each. In the first experiment, the first group was injected with physiological saline and the second and third groups were intramuscularly given ketamine at a dose level of 5 mg/kg B.W. and 15 mg/kg B.W., respectively. In the second experiment, the first and second groups were given ketamine at a dose of 5 mg/kg B.W. and of 15 mg/kg B.W., respectively, and the third group was served as control injected with saline. In the third experiment, the first and third groups were administered with 15 mg/kg and 5 mg/kg of ketamine and the second group was injected with saline. In short, all of the twenty monkeys received the three different treatments for two months. The serum prolactin level showed a marked increase after the administration of ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Radioimmunoassay of haloperidol in human serum: Correlation of serum haloperidol with serum prolactin

A radioimmunoassay (RIA) for measurement of serum haloperidol is described. Compared to gaschromatography (GC), RIA values average 40% higher. However, a simple organic extraction of serum yields statistically equivalent RIA and GC haloperidol determinations. For both men and women combined, there was a positive correlation between dose (mg/kg/day) and steady-state serum haloperidol level (r = +0.86) and between steady-state serum haloperidol and serum prolactin (PRL) concentration (r = +0.87).     

Long-term cimetidine does not alter serum prolactin.

The effect of repeated cimetidine ingestion on serum prolactin values was studied prospectively in 17 men with proven duodenal ulcers. These patients received 400 mg of cimetidine twice daily for 12 weeks but showed no alteration in their mean serum prolactin levels. Cimetidine-induced hyperprolactinaemia is not the explanation for the development of gynaecomastia in men exposed to this drug.     

Carbidopa elevates hypothalamic dopa and serum prolactin in rats.

The administration of carbidopa (MK-486, α-methyl-L-dopa hydrazine; 100–200 mg/kg, intraperitoneally) causes several-fold increases in hypothalamic dopa and serum prolactin levels in male rats within 2 hours; these changes are not reversed by the administration of pyridoxine. These observations suggest that high doses of carbidopa can affect catecholamine synthesis within the hypothalamus.