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PubMed2002

A prospective, double-blind, randomized, placebo-controlled clinical trial of bromocriptin in clomiphene-resistant patients with polycystic ovary syndrome and normal prolactin level.

OBJECTIVE: The purpose of this study was to examine the effects of of bromocriptin combined with clomiphene citrate in clomiphene-resistant patients with polycystic ovary syndrome and normal prolactin level. DESIGN: Prospective, double-blind, controlled study. SETTING: University teaching hospital. PATIENTS: One hundred polycystic ovary patients and normal prolactin (PRL) who were clomiphene citrate resistant. INTERVENTIONS: Treatment group received 150 mg clomiphene citrate on days 5-9 and 7.5 mg bromocriptin continuously. Control group received the same protocol of clomiphene citrate combined with placebo. MAIN OUTCOME MEASURES: Hormonal status, follicular monitoring, ovulation rate. RESULTS: Follicular development (follicular size greater than 15 mm) was observed in 12 (25.5%) and eight (15.1%) women in treatment and placebo group respectively ( P=0.29). The serum prolactin level was within normal limits in all patients before treatment. After 3 and 6 months of treatment with bromocriptin, there was a significant decrease in serum level of prolactin ( P=0.000001). No any significant differences was seen in ovulation, and serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), dehydroepiandrosterone sulfate (DHEAS), progesterone (P) between treatment and placebo group after treatment. CONCLUSIONS: The only significant effect of long-term bromocriptin therapy in clomiphene citrate resistant polycystic ovary women was to lower the serum prolactin concentration. It was also concluded that 10-15% of patients with polycystic ovaries experienced occasional ovulatory cycles and pregnancy whether or not they were on treatment.

Adult↗
PubMed1982

Bromocriptine treatment of women with suspected pituitary prolactin-secreting microadenomas.

The present study was designed to investigate the efficacy of bromocriptine in reducing serum prolactin (PRL) levels and in decreasing the size of PRL-secreting microadenomas. Bromocriptine, 5.0 mg, was administered daily for 2 years of 17 women who had galactorrhea, hyperprolactinemia, and hypocycloidal polytomographic evidence suggestive of a pituitary microadenoma. Serum PRL levels were normalized in 16 of 17 women during therapy. Associated with this was resumption of regular menses in 15 of 16 women with menstrual dysfunction and cessation of galactorrhea in 16 of the 17 women. Improvement in the roentgenographic appearance of the sella turcica occurred in two women. No progression in tumor size was found during the course of therapy. Side effects attributed to bromocriptine were minimal, transient, and usually well tolerated. These data suggest that bromocriptine is an appropriate therapeutic modality for PRL-secreting pituitary microadenomas.

Adenoma↗
PubMed1989

Acute and subchronic effects of low-dose bromocriptine in haloperidol-treated schizophrenics.

The effects of the acute (within 24 hr) and subchronic (21 days) addition of low-dose bromocriptine (2.5 mg/day) were compared to placebo in schizophrenic patients treated concomitantly with haloperidol. After 24 hr patients on bromocriptine (n = 15) showed a mean improvement of 29% in the total score of the Brief Psychiatric Rating Scale (BPRS) as compared to 14% in the placebo group (n = 15) (p less than 0.10). The acute improvement correlated negatively with bromocriptine plasma levels; patients with the highest reduction in BPRS score had the lowest plasma levels (between 50 and 150 pg/ml) at 60, 90, and 120 min after intake. The improvement in the bromocriptine group continued until the 10th day of the trial, when a nonsignificant increase in the total BPRS score took place. Analysis of Variance of the overall BPRS improvement during the 21 days revealed no significant difference between both patient groups. Our results give modest support to the idea of an acute antipsychotic response to low-dose dopamine agonists in neuroleptic-treated patients, but fail to support their clinical usefulness in the subchronic treatment of schizophrenia.

Adult↗
PubMed1994

Bromocriptine protects mice against 6-hydroxydopamine and scavenges hydroxyl free radicals in vitro.

Pretreatment with bromocriptine (5 mg/kg, i.p., 7 days) completely protected against the decrease in mouse striatal dopamine and its metabolites induced by intraventricular injection of 6-hydroxydopamine after intraperitoneal administration of desipramine, but similar pretreatment with L-DOPA/carbidopa (75/7.5 mg/kg, i.p., 7 days) showed only partial protective effect. Furthermore, in an in vitro system that generated.OH from FeSO4-H2O2, bromocriptine dose-dependently reduced the number of .OH radicals. These findings indicate that bromocriptine has a neuroprotective effect against neurotoxins such as 6-hydroxydopamine, probably due, in part, to its hydroxyl radical scavenging activity and inhibiting effect on dopamine turnover rate. This suggests that early introduction of bromocriptine in the therapy of Parkinson's disease may be superior to treatment with L-DOPA alone.

Animals↗
PubMed1979

Analysis of the effects of bromocriptine on blood pressure and sympathetic nerve function.

Bromocriptine, a dopamine receptor agonist, lowered arterial blood pressure and caused significant impairment of the cardioacceleration observed during the stimulation of the right postganglionic cardiac sympathetic nerve fibers in pentobarbital-anethetized dogs. Prior administration of pimozide antagonized the hypotensive and the inhibitory action of bromocriptine on cardiac sympathetic function. These results suggest that while presynaptic dopamine receptors seem to be involved in mediating the inhibitory action of bromocriptine on cardiac sympathetic function, the role of presynaptic as well as dopamine receptors located at other sites in mediating the hypotensive action of bromocriptine needs to be further investigated.

Animals↗
PubMed1983

Autoreceptors mediate the inhibition of dopamine synthesis by bromocriptine and lisuride in rats.

The administration of bromocriptine and lisuride to rats caused a decrease in striatal dopamine (DA) synthesis, as measured by 3,4-dihydroxy-phenylalanine (DOPA) accumulation after decarboxylase inhibition. DOPA formation was inhibited by a maximum of about 60% of control values by bromocriptine and lisuride, 5.0 and 0.3 mg/kg, respectively. Both compounds showed very similar time-courses for the effect and failed to modify DOPA accumulation during the first 30 min. Pretreatment with (-)-sulpiride (50 mg/kg i.p.), a specific D2-receptor blocker, completely prevented the inhibitory effect of bromocriptine and lisuride on DOPA accumulation. Finally, both compounds significantly reversed the gamma-butyrolactone (GBL) (700 mg/kg i.p.)-induced DOPA accumulation at doses (0.25 and 0.015 mg/kg, respectively) that were inactive in normal rats. The data suggest that bromocriptine and lisuride act as agonists on D2-presynaptic autoreceptors which have different sensitivity to the agonist according to the basal firing rate of DA neurons.

4-Butyrolactone↗
PubMed1983

Bromocriptine inhibits 2-deoxy-D-glucose-stimulated gastric acid secretion in the rat.

The influence of bromocriptine on the secretagogue-induced gastric acid secretion was examined in rats. The drug inhibited the gastric acid secretion centrally stimulated by 2-deoxy-D-glucose (2DG) in anesthetized or conscious rats. Apomorphine also prevented 2DG-induced acid secretion in anesthetized rats but not in conscious rats. Neither bromocriptine nor apomorphine significantly influenced the acid secretion induced peripherally by electrical vagus stimulation or gastrin. The antisecretory effect of bromocriptine was reversed by dopamine antagonists in anesthetized or conscious rats, but not by apomorphine in anesthetized rats. The results suggest that in rats, the antisecretory effect of bromocriptine on 2DG-stimulated acid secretion is partly due to its central dopamine agonistic action, but that of apomorphine may be due to dopaminergic plus other mechanisms.

Animals↗
PubMed1994

Induction of apoptosis in murine ACTH-secreting pituitary adenoma cells by bromocriptine.

Bromocriptine, a dopamine agonist, is now an accepted primary therapeutic agent for patients with prolactinomas and other pituitary adenomas. In this study, we demonstrated that bromocriptine inhibited the proliferation of murine ACTH-secreting pituitary adenoma (AtT-20) cells. In addition, the antitumor activity of bromocriptine was inhibited both by actinomycin D and cycloheximide, suggesting that it was dependent on new RNA and protein synthesis. Interestingly, the results of DNA fragmentation assays and cell cycle analysis clearly demonstrated that bromocriptine induced apoptosis in AtT-20 cells.

Adenoma↗
PubMed1984

Seasonal patterns of circulating progesterone and prolactin and response to bromocriptine in the female tammar Macropus eugenii.

Concentrations of prolactin and progesterone in the plasma of female tammars (Macropus eugenii) were measured during lactational quiescence and seasonal quiescence and during the period of natural resumption of reproduction after the summer solstice in December. Prolactin concentrations were consistently low (less than 40 ng/ml) during the period of declining day length and consistently elevated (greater than 40 ng/ml) during the period of increasing day length. Basal levels of progesterone were lowest (118.9 +/- 9.1 pg/ml) at the winter solstice and highest (244.1 +/- 21.0 pg/ml) at the summer solstice. Treatment with bromocriptine (CB154) did not depress prolactin levels at either time of the year but during February to June a single injection of 5 mg/kg body wt induced development of the quiescent corpus luteum (CL) and the diapausing embryo was reactivated. In February and March the level of progesterone increased in association with the developing CL, but after treatment at the winter solstice in June plasma progesterone did not increase although pregnancy was successfully completed. From September through November only 1 of 50 females responded to bromocriptine. None responded to bromocriptine given at the summer solstice in December, but all these animals spontaneously reactivated 2 weeks later. The difference in response of female tammars to bromocriptine treatment in the two halves of the year suggests that different endocrine controls operate in lactational and seasonal quiescence and that the latter is more complex.

Animals↗
PubMed1985

Mechanism of bromocriptine-induced hyperglycaemia.

Results reveal that bromocriptine at a dose of 6 mg/kg. I.P. in mice caused a significant hyperglycaemic effect which was accompanied by a marked increase in liver glycogen. After adrenalectomy, the effect of bromocriptine on serum glucose level was reduced whereas its effect on liver glycogen content was abolished. In rats, administration of bromocriptine (17.5 mg/kg I.P.) induced a significant rise in serum glucose level which was associated with marked reduction in serum insulin activity and increase in serum corticosterone level with no effect on serum triiodothyronine (T3) or thyroxine (T4) levels. It could be concluded that bromocriptine-induced hyperglycaemia might be attributed at least partially to inhibition of insulin release and stimulation of corticosterone secretion.

Adrenalectomy↗
PubMed1989

Reductions of body fat stores and total plasma cholesterol and triglyceride concentrations in several species by bromocriptine treatment.

Administrations (injections and in feed) of bromocriptine, a dopamine agonist that inhibits prolactin secretion, reduced body fat stores and plasma total cholesterol and triglyceride concentrations in several rodent species (Syrian hamsters, Djungarian hamsters, Swiss Webster mice and obese Zucker rats). Body fat indices were reduced by at least 50% in the hamsters and mice within 10-15 days of treatment and by 29% in 8 weeks in the rats. Bromocriptine reduced total plasma cholesterol concentration by 17% in Syrian hamsters, 41% in mice and 30% in rats fasted before blood sampling. In nonfasted obese rats, bromocriptine dramatically reduced both cholesterol (from 440 to 130 mg/dl) and triglyceride (from 1570 to 540 mg/dl) levels compared with controls. These findings offer further evidence for a primary role of prolactin in lipid metabolism and indicate that bromocriptine may be useful for treating obesity and lipid-based cardiovascular disorders.

Adipose Tissue↗
PubMed1981

Lactation-inhibiting and prolactin-lowering effect of lisuride and bromocriptine: a comparative study.

The prolactin-lowering and lactation-inhibiting effects of lisuride and bromocriptine, two dopaminergic drugs, were compared in a double-blind study. Twenty-six women took lisuride, 0.2 mg b.i.d., and 24 women took bromocriptine, 2.5 mg b.i.d., during 14 days postpartum. Though both drugs gave satisfactory inhibition of puerperal milk production, in these dosages bromocriptine was a more effective lactation inhibitor and prolactin suppressor. After discontinuation of treatment rebound symptoms were more pronounced in the bromocriptine group than in the lisuride group.

Bromocriptine↗
PubMed1987

D-1 dopamine receptor stimulation potentiates neurophysiological effects of bromocriptine in rats with lesions of the nigrostriatal dopamine pathway.

Neurophysiological techniques were used to examine the possibility that the effects of bromocriptine, a direct acting dopamine agonist, can be potentiated by D-1 receptor stimulation in an animal model of parkinsonism. Single unit activity of substantia nigra pars reticulata neurons was recorded in rats with 6-hydroxydopamine induced lesions of the nigrostriatal pathway. The results showed that the coadministration of bromocriptine with the selective D-1 agonist SKF 38393 greatly attenuated pars reticulata neuronal activity at doses that did not produce significant effects when administered alone. Thus, processes elicited by D-1 receptor stimulation and bromocriptine exert synergistic effects in these 6-hydroxydopamine lesioned rats. This observation may be relevant to the mechanism underlying l-DOPA's ability to potentiate the therapeutic effects of bromocriptine in parkinsonian patients.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Bromocriptine-induced cerebrospinal fluid fistula in patients with macroprolactinomas: report of three cases and a review of the literature.

Bromocriptine therapy for macroprolactinoma induced cerebrospinal fluid (CSF) rhinorrhea in three patients. The tumor had extended well beyond the sella turcica and caused bony erosion in all the cases. All three patients responded to bromocriptine therapy rapidly. CSF fistula occurred concomitantly with the reduction of tumor size and caused meningitis in two of the patients. Withdrawal of bromocriptine resulted in cessation of the leakage. One of the patients underwent transsphenoidal repair. Two patients refused surgery. This potentially lethal complication encountered in these three cases demonstrates the need for close supervision of macroprolactinoma patients with skull base erosion placed under bromocriptine therapy.

Adult↗
PubMed1994

Effects of bromocriptine and haloperidol on ethanol withdrawal syndrome in rats.

The effects of bromocriptine and haloperidol, either alone or in combination, on ethanol withdrawal syndrome (EWS) have been investigated in rats. Bromocriptine (5 mg/kg 1P) inhibited wet dog shakes behavior and catatonia but potentiated the intensity of abnormal gait. The latency of the audiogenic seizures was prolonged by bromocriptine treatment. Haloperidol (0.5 mg/kg SC) decreased the intensity of stereotyped behavior but potentiated catatonia and agitation. It did not antagonize the behaviors induced by bromocriptine when injected in combination except the increased latency of the audiogenic seizures. The total intensity score of the EWS was not significantly different from that in untreated control. The results suggest that brain dopaminergic system may be involved to a limited extent in mediating the EWS in rats.

Acoustic Stimulation↗
PubMed1981

Bromocriptine and imipramine in endogenous depression. A double-blind controlled trial in out-patients.

Among 33 out-patients with endogenous depression, 16 were treated with bromocriptine (10-60 mg/day, mean 34) and 17 with imipramine (75-250 mg/day, mean 143). The total score on the Hamilton Rating Scale decreased during 6-week treatment from 19.9 to 7.8 in the bromocriptine group (P less than 0.001) and from 20.1 to 6.1 in the imipramine group (P less than 0.001). There was no significant difference between the two groups. The main side-effects were for bromocriptine: nausea, dizziness, and headache; for imipramine; dryness of mouth, dizziness, and sweating. This study suggests an antidepressant effect of bromocriptine although, due to the possibility of Type II error, it may not necessarily be equal to that of imipramine.

Adolescent↗
PubMed1987

Single-dose bromocriptine reverses cocaine craving.

Thirteen hospitalized cocaine addicts complaining of cocaine craving were given a single dose of bromocriptine, a dopamine agonist, in a randomized, double-blind, placebo-controlled study design. Compared to placebo, bromocriptine caused a significant reduction in craving ratings. These data suggest that bromocriptine may be effective as a new, nonaddictive pharmacological treatment for cocaine addicts and support the notion that functional dopamine depletion occurs with chronic cocaine use. Open trials indicate that low-dose bromocriptine may be useful in cocaine detoxification.

Adult↗
PubMed1988

The effect of bromocriptine on the lactotroph cells in two inbred strains of mice C3H/Sy and AKR/Sy.

This paper deals with the effect of bromocriptine on the morphology and the number of lactotrophs in two inbred strains of mice, one with a high and the other with a low mammary cancer incidence. Bromocriptine decreases the number of lactotrophs in C3H mice while their number in AKR is not affected. These observations suggest that bromocriptine affects the two strains in a different way, probably due to their different prolactin levels in the pituitary. The above treatment resulted also in a shrinking of the RER and a reduction in size of prolactin granules, probably due to a decline in the secretory activity of lactotrophs. Of special interest was the appearance of a 'new' cell type with mixed characteristics of somatotrophs and lactotrophs. These findings, along with an increase in the number of chromophobes, suggest that bromocriptine can induce cell regression. Probably the 'new' cell is an intermediate form between chromophobes and lactotrophs and somatotrophs.

Animals↗