PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Bromocriptine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

[Effects of repeated administration of bromocriptine on ambulatory activity in mice, and changes in methamphetamine sensitivity in bromocriptine-experienced mice].

Effects of repeated administration of bromocriptine, a long-acting dopamine agonist, as well as interaction between bromocriptine and methamphetamine were investigated by mean of ambulatory activity in mice. The ambulatory activity of each mouse was measured by a tilting-type activity cage for 6 and 3 hr after administration of bromocriptine and methamphetamine, respectively. The repeated 5 times administration of bromocriptine and of methamphetamine was at intervals of 7 days and of 3-4 days, respectively. Bromocriptine tended to suppress the activity at low doses (1 and 2mg/kg, ip), but increased the activity at high doses (8 and 16 mg/kg, ip), showing biphasic effects depending on the doses administered. Both the ambulation-suppressing and -increasing effects of bromocriptine were enhanced when the drug was repeatedly administered. The mice that experienced the repeated administration of low doses and high doses of bromocriptine exhibited a decrease and an increase, respectively, in the sensitivity to the ambulation-increasing effect of methamphetamine (2 mg/kg, sc). Repeated administration of methamphetamine (2 mg/kg, sc) elicited an increase in sensitivity not only to methamphetamine itself, showing reverse tolerance, but also to high doses of bromocriptine, showing cross reverse tolerance. However, the reverse tolerance to methamphetamine, once produced, was not affected by the repeated administration of low doses of bromocriptine.

Animals↗

Ropinirole versus bromocriptine for levodopa-induced complications in Parkinson's disease.

BACKGROUND: Long-term levodopa therapy for Parkinson's disease is complicated by the development of motor fluctuations and abnormal involuntary movements. One approach is to add a dopamine agonist at this stage of the disease to reduce the time the patient spends immobile or off and to reduce the dose of levodopa in the hope of reducing such problems in the future. OBJECTIVES: To compare the efficacy and safety of adjuvant ropinirole therapy with bromocriptine in patients with Parkinson's disease already established on levodopa therapy and suffering from motor complications. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with SmithKline Beecham. SELECTION CRITERIA: Randomised controlled trials of ropinirole versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data was abstracted independently by the authors and differences settled by discussion. The outcome measures used included Parkinson's disease rating scales, levodopa dosage, 'off' time measurements and the frequency of withdrawals and adverse events. MAIN RESULTS: No significant differences between ropinirole and bromocriptine were found in off time reduction, dyskinesia as an adverse event, motor impairment and disability, or levodopa dose reduction. Withdrawal rates and adverse event frequency were similar with the two agents apart from significantly less nausea with ropinirole (odds ratio 0.50; 0.29, 0. 84 95% CI; p =0.01). REVIEWER'S CONCLUSIONS: Ropinirole is at least as good as bromocriptine in patients with Parkinson's disease with motor complications in terms of improving off time and reducing levodopa dose, without increasing adverse events including dyskinesia. However, these comparitor studies may have been underpowered to detect clinically meaningful differences between the agonists. Further, much larger, phase IV studies are required to examine the efficacy, effectiveness, and safety of all of the dopamine agonists as adjuvant therapy in Parkinson's disease.

Antiparkinson Agents↗

Bromocriptine suppression of TRH-stimulated prolactin and thyrotrophin release and accompanying inhibition of bromocriptine induced growth hormone release by TRH in normal man.

Six normal fasting males received on four separate occasions in random order (1) a placebo tablet followed 60 min later by 200 microgram of TRH intravenously (2) bromocriptine 2.5 mg orally followed by TRH intravenously (3) bromocriptine 2.5 mg orally followed by a placebo injection and (4) placebo tablet followed by placebo injection. Plasma prolactin and TSH responses to TRH were decreased following bromocriptine pretreatment. The rise of plasma growth hormone after bromocriptine was inhibited by TRH. The rise in plasma FSH seen after TRH injection was not influenced by bromocriptine pretreatment. Circulating LH and insulin concentrations were unaffected by any drug administration. These results suggest a dopaminergic influence on prolactin and TSH release in normal men, an inhibitory effect of TRH on bromocriptine stimulated growth hormone secretion, and no dopaminergic modulation of basal insulin secretion.

Adult↗

[Prolactin, bromocriptine and gonadal function in women: recent advances. II. Treatment of female hyperprolactinemia and other indications for the use of bromocriptine].

The surgical treatment of prolactinomas protects against the complications that these tumours have, but by itself does not cure the infertility which is found in at most 50% of all cases. The value of radiotherapy is limited to those cases where there is a contra-indication for carrying out surgery and in the tumours that have been incompletely removed and when pregnancy is not desired. The principal drugs used to lower prolactin are the dopamine agonist, which is bromocriptine and the serotonin antagonist which is methergoline which is less powerful than bromocriptine. Bromocriptine brings about normal prolactinaemia and ovulation is re-established and menstruation returns in most cases of idiopathic hyperprolactinaemia and in many cases where hyperprolactinaemia is due to a tumour. It, in certain cases, has an antitumoral effect and can definitely cure some hyperprolactinaemias whether they are tumoral or not. So bromocriptine is the specific treatment of women whose sterility is due to hyperprolactinaemia and no teratogenic effect has been reported. The only complications that have occurred in pregnancies that have been induced by this drug have been growths in the tumours in women who have pituitary adenomata, but these complications are far less frequent and serious in cases of micro-adenomata. Since the antitumoral effect of bromocriptine has been discovered the indications for surgery have lessened but it is often all the same necessary. The medical treatment of adenomata can only be considered when strict supervision is going to be undertaken. Bromocriptine can also establish ovulation in a few categories where ovulation occurs in normoprolactinaemic women and it can also be used as a treatment for the premenstrual syndrome.

Anovulation↗

Pharmacokinetic and pharmacodynamic analyses, based on dopamine D2-receptor occupancy of bromocriptine, of bromocriptine-induced contralateral rotations in unilaterally 6-OHDA-lesioned rats.

Bromocriptine is a selective agonist for dopamine D2-receptors and is used in the treatment of Parkinson's disease. In this study, we performed pharmacokinetic and pharmacodynamic (PK/PD) analyses of the antiparkinsonian effect of bromocriptine and evaluated drug-induced contralateral rotations in rats in which unilateral striatal lesions had been generated by microinjection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. The plasma concentration (Cp) and D2 receptor occupancy (Phi(D2)) were quantitated by HPLC and with an in vivo back-titration method using [(3)H]-raclopride, respectively. Bromocriptine induced contralateral rotations (E(rot)) in a dose-dependent manner following intraperitoneal administration in an animal model of Parkinson's disease. The Cp of bromocriptine peaked at 15-30 min after the administration and decreased time-dependently, whereas the Phi(D2) of bromocriptine increased gradually for 180 min after administration. The relationship between Cp and E(rot) exhibited an anticlockwise hysteresis, whereas the relationship between Phi(D2) and E(rot) showed a linear correlation. These results suggest that in vivo Phi(D2) is a good pharmacological indicator of the effect of a D2 agonist.

Animals↗

Bromocriptine self-administration and bromocriptine-reinstatement of cocaine-trained and heroin-trained lever pressing in rats.

Rats were trained to lever press for intravenous cocaine (1.0 mg/kg/injection) and then switched to bromocriptine (0.3, 1.0, or 3.0 mg/kg/injection) on a FR-1 reinforcement schedule. Bromocriptine sustained responding at all three doses; hourly drug intake increased linearly with log-dose. In a second experiment, animals were trained to respond for cocaine (1.0 mg/kg/injection) or heroin (0.1 mg/kg/injection) reinforcement; drug was available for the first 2 h of each daily session; saline was substituted for cocaine or heroin for 5 subsequent hours. One hour into each saline substitution session, an intravenous injection of saline or bromocriptine (0.0, 0.5, 1.0, or 2.0 mg/kg) was given. Bromocriptine reinstated both cocaine-trained and heroin-trained lever pressing; under these conditions, the drug was most effective in the heroin-trained animals. Reinforcing doses of clonidine (0.0625 and 0.125 mg/kg), methohexital, and nicotine (0.05 and 0.1 mg/kg), and a sub-intoxicating dose of ethanol (2 g/kg) failed to reinstate cocaine-trained responding. These data indicate that bromocriptine has cocaine-like and heroin-like stimulus and reinforcing effects.

Animals↗

Double-blind comparison of pramipexole and bromocriptine treatment with placebo in advanced Parkinson's disease. International Pramipexole-Bromocriptine Study Group.

Pramipexole is a new, selective, nonergoline dopamine agonist that acts on D2 and preferentially on D3 dopamine receptors. Phase II and III clinical trials have shown this drug to be useful in treating both early and advanced Parkinson's disease (PD) patients. A double-blind, randomized, multicenter study was performed to compare the safety, tolerance, and efficacy of pramipexole versus placebo in patients with advanced PD with motor fluctuations. A bromocriptine treatment group was included to enable comparisons between bromocriptine and placebo groups, but the study was not powered to show statistical differences between the active treatment groups. The study included 247 patients with "wearing off." Patients were Hoehn and Yahr stages II to IV during "on" times. The trial included three phases: dose escalation, 6 months' maintenance, and dose reduction. The primary end points were the Unified Parkinson's Disease Rating Scale (UPDRS) parts II and III. Up to 4.5 mg per day of pramipexole and 30 mg per day of bromocriptine were used. The results of the study showed that the UPDRS part II improved by 26.7% for pramipexole (p = 0.0002) and 14% for bromocriptine (p = 0.02) versus 4.8% for placebo. The UPDRS part III showed improvements of 34% for pramipexole (p = 0.0006) and 23.8% for bromocriptine (p = 0.01) versus 5.7% for placebo. There were no major differences in safety data. In the active treatment groups there were more reports of dyskinesia and nausea compared with placebo. In regard to comparison of the Global Clinical Assessment of Efficacy between active treatment groups, there was a trend to significance (p = 0.056) in favor of pramipexole. We conclude that pramipexole-treated patients with advanced PD improved significantly more than placebo for both primary end points.

Adult↗

Nerve growth factor and bromocriptine: a sequential therapy for human bromocriptine-resistant prolactinomas.

Nerve growth factor (NGF) administration to athymic mice with transplanted human bromocriptine-resistant prolactinoma, results in the expression of dopamine D-2 receptors in the tumour and restores sensitivity to subsequent treatment with bromocriptine, which then produces normalisation of plasma prolactin and tumour regression. Sequential administration of NGF and bromocriptine thus may be a promising therapy for patients refractory to bromocriptine.

Animals↗

Bromocriptine as initial therapy in elderly parkinsonian patients. The Bromocriptine Multicentre Trial Group.

The problems of long-term levodopa treatment are well established, and a number of studies describe the use of bromocriptine as a first-line agent in patients under 65 years. This multicentre double-blind study compared the efficacy of low and very low dose bromocriptine in 64 elderly subjects with newly diagnosed Parkinson's disease. Both regimens led to clinical improvement, but there was a high drop-out rate and a high mortality. These difficulties, together with a low recruitment rate, resulted in problems of statistical analysis. There was no significant advantage in using the higher of the two dosage regimens, and we would recommend a maintenance dosage range of 5 mg-15 mg bromocriptine daily. On the basis of this study, however, bromocriptine seems unlikely to replace levodopa as the first-line treatment for Parkinson's disease.

Aged↗

Sensitive and specific bromocriptine radioimmunoassay with iodine label: measurement of bromocriptine in human plasma.

Plasma bromocriptine assays must have high sensitivity because plasma concentrations are low, and high specificity because bromocriptine is extensively metabolised. This paper describes the simple preparation of a radioiodine-labelled derivative of dihydroergocriptine and its use in a radioimmunoassay employing an antiserum directed against the intact bromocriptine molecule. The method could measure plasma bromocriptine at concentrations of 0.05 nmol/L, had between-assay coefficients of variation of less than 10% and was more convenient than previous assays using tritium radiolabels.

Adenoma↗

Non-functioning pituitary adenomas do not regress during bromocriptine therapy but possess membrane-bound dopamine receptors which bind bromocriptine.

Dopaminergic binding to membranes from 20 well-characterized non-functioning pituitary tumours was investigated using the radioligand [3H]spiperone; nine had failed to regress during pre-operative bromocriptine therapy. Five macroprolactinomas and six normal pituitaries were similarly investigated. High affinity dopaminergic binding sites were defined in all tissues studied. Mean dissociation constants were similar for the three groups (0.92, 0.55 and 0.51 nmol/l, respectively) but mean site numbers were greater in the prolactinomas (698) than in non-functioning tumours (131) or normal pituitaries (136 fmol/mg protein). In a pool of non-functioning tumour membranes ligand competition experiments confirmed that binding was dopaminergic. Stereospecificity was demonstrated using the (+) and (-)isomers of butaclamol. Bromocriptine was present in three non-functioning tumours that had been exposed to the drug within 24 h of surgery and it largely prevented [3H]spiperone binding; membrane washing restored [3H]spiperone binding to control values. We conclude that non-functioning tumours possess high affinity membrane-bound dopaminergic binding sites similar to those in normal pituitary and macroprolactinomas, but apparently fewer in number than in the latter. Though bromocriptine binds to dopamine receptors on non-functioning tumours in vivo, this does not result in tumour regression.

Adenoma↗

Bromocriptine in Parkinson's disease: a double-blind study comparing "low-slow" and "high-fast" introductory dosage regimens in de novo patients. UK Bromocriptine Research Group.

One hundred and thirty four patients with previously untreated Parkinson's disease were recruited to a multicentre double blind study comparing two introductory dosage regimens of bromocriptine: a low/slow regimen increasing to a maximum of 25 mg/day and a high/fast regimen increasing to a maximum of 100 mg/day over a 26 week period. It was hoped to determine the minimum dose of bromocriptine required with either regimen. A patient's ability to achieve a 33% improvement in clinical rating scores was recorded using a combined score of functional disability (Webster) and self rated daily living activities (ADL). Sixty five out of 129 patients (50%) had reached the improvement criteria in 26 weeks, 37 (49%) from the "slow" and 28 (53%) from the "fast" group (N.S.). However, if only those patients still in the trial at the end of 26 weeks are considered the relevant percentages are 73% and 88% (p less than 0.05). Statistical analysis allowing for censored observations was used to examine group differences in dosage and time at improvement. This excluded the patients who had dropped out due to side effects from the calculations. The results indicated a marked difference between groups in both dose (slow 22.0 mg, fast 55.4 mg (p less than 0.01) and time (slow 22.8 weeks and fast 14.4 weeks (p less than 0.05). Severe side effects necessitated withdrawal from the trial in 34 patients, a larger proportion 19 (36%) being in the fast group compared with 15 (20%) from the slow group (p less than 0.05). The number of dropouts due to non effect was 2 (4%) in the fast and 10 (13%) in the slow. The only predisposing factor relating to dropping out due to side effects was a high initial ADL (p < 0.01). It is concluded that bromocriptine is an effective de novo treatment for Parkinson's disease. The "fast" introductory regimen is less well tolerated than the "slow", but the later has the disadvantage of a long delay before patients reach an effective dose. It is recommended that it would be wise to adopt an intermediate dosing strategy.

Bromocriptine↗

Comparison between a slow-release oral preparation of bromocriptine and regular bromocriptine in patients with hyperprolactinemia: a double blind, double dummy study.

The efficacy and tolerability of a slow-release preparation of bromocriptine (Parlodel SRO) were compared to those of conventional bromocriptine (Parlodel R) in a double blind, double dummy study of 12 hyperprolactinemic women (plasma PRL 81.3 +/- 4.73, ng/ml mean +/- SEM). For 2 weeks, the patients received 2.5 mg b.i.d. Parlodel R or 5 mg once daily Parlodel SRO; for the following 2 weeks, the dose of the drugs was doubled. The patients were then treated, in an open study, with 2.5-10 mg daily Parlodel SRO for 6 months. Both preparations caused a prompt and sharp PRL fall. Hormone levels remained inhibited over the whole month of observation with both preparations. Daily PRL profiles were very close with either drug although morning PRl levels were slightly higher during Parlodel SRO than during Parlodel R administration. Doubling the doses of the two drugs did not result in further significant lowering of PRL values. During the 6-month study with Parlodel SRO, plasma PRL further decreased and normalized in 11 of 12 patients. Clinical improvement occurred in the majority of cases. Tolerability of Parlodel SRO appeared to be better, though without statistically significant differences, than that of Parlodel R. Side effects were less important with the former compound in their number, severity and duration. In conclusion, thanks to its favourable pharmacological profile, Parlodel SRO appears to be a valuable alternative to regular bromocriptine in the management of hyperprolactinemia.

Administration, Oral↗

[Effect of bromocriptine and bromocriptine combined with prolactin on the proliferation of thymocytes in young rats].

The effects of bromocriptine and bromocriptine associated to prolactin have been investigated on young rat thymocytes after sensitization with T-cell antigen SRBC using a quantitative nucleus image analysis (Samba 200). Bromocriptine alone induces an inhibition of lymphocyte proliferation, a chromatin condensation and enhances cell differentiation. These effects are reversed by prolactin, which therefore acts on lymphocytes before they leave the thymus.

Animals↗

Counteraction of the haloperidol blockade of ovulation by bromocriptine, and the effect of bromocriptine on LH and prolactin secretion.

Previous experiments showed that haloperidol (Haldol) blocked LH release and ovulation when injected on the day of proestrus in the female rat. The present studies were designed to investigate the mechanism of Haldol blockade and the possibility that bromocriptine (CB) might counteract the effect. One hour prior to subcutaneous injection of an effective dose of Haldol (0.25 mg/kg at 09.30 h), CB was injected intraperitoneally at one of four doses (2.5, 5.0, 7.5, or 10.0 mg/kg at 08.30 h). Bromocriptine was effective at restoring LH release and ovulation, and the optimal dose for this particular experiment was found to be 7.5 mg/kg. The highest dose (10.0 mg/kg), however, resulted in no significant increase in ovulation. Treating animals with CB (5.0, 10.0, or 20.0 mg/kg at 08.30 h) followed by control vehicle showed that high doses of CB caused a significant inhibition of LH release and ovulation. After 20.0 mg/kg there was no significant surge of LH, and although ovulation did occur it was significantly suppressed when compared to control animals (p = 0.017). These results showed that appropriate doses of CB counteract the Haldol blockade of LH release and ovulation. The suppression of Haldol-induced PRL secretion by low-dose CB, without the significant restoration of ovulation, supported the hypothesis that the Haldol blockade was mediated via a direct effect of Haldol on central nervous system control mechanisms. While CB alone exerted a profound inhibition of PRL at low doses, it had no effect on LH release. CB at high doses, however, was inhibitory to both LH release and ovulation.

Animals↗

Perifusion studies of bromocriptine-treated and untreated macroprolactinomas: effects of dopamine, bromocriptine and TRH.

There have been no detailed in-vitro studies of PRL secretion by human macroprolactinoma cells exposed to bromocriptine (BC) to within a few days of surgical removal. We have studied cells from four such tumours (serum PRL 7.05-247 U/l) and six untreated tumours (serum PRL 4-80.35 U/l) using a perifusion technique. The BC-treated tumours had shown tumour shrinkage and were treated until 40-96 h before surgery, but in one patient serum PRL had not suppressed below 15 U/l despite chronic treatment. Pretreatment serum PRL responses to TRH were blunted in all 10 patients. During perifusion with dopamine (DA, 5 mumol/l) untreated prolactinomas had a higher PRL secretion rate (19.3 +/- 2.7 microU/mg tissue/min, mean +/- SEM) than BC-treated (3.9 +/- 0.7, P = 0.005). When DA was removed, PRL secretion from untreated tumours increased to 129.7 +/- 18.7 microU/mg/min, but in three of the BC-treated, little increase occurred. In the fourth (from the patient whose serum PRL had not fully suppressed) PRL secretion increased from 4.4 to 25.6 microU/mg/min after DA withdrawal, and DA and BC dose-related inhibition of PRL was similar to that observed in untreated tumours. TRH (10 ng/ml), without DA, provoked increased PRL release from both untreated (266% basal secretion, n = 3) and BC-treated (298%, n = 3) tumours; this effect was completely inhibited by DA (5 mumol/l). The absence of hormones other than PRL following potassium (55 mmol/l) excluded contaminating normal pituitary. We conclude: (1) The effects of BC on prolactinoma PRL secretion may persist for at least 4 days; (2) partial in-vivo BC resistance can be due to factors other than DA receptor malfunction; (3) the apparent discrepancy between in-vivo and in-vitro TRH responses was consistent with the presence of increased hypothalamic DA tone in vivo; and (4) BC may have differential effects on TRH and DA-controlled PRL pools in the tumourous lactotroph.

Bromocriptine↗

[Combined therapy of bromocriptine, clomiphene citrate and HMG in normoprolactinemic amenorrhea patients who fail to respond to bromocriptine-clomiphene citrate therapy].

The purpose of this study is to investigate the ovulatory effect of the following three methods on 40 patients with normoprolactinemic amenorrhea patients who failed to respond to clomiphene citrate (Cl) alone. Method I is the combined therapy with bromocriptine and Cl (Brc/Cl). Method II is the combined therapy with Brc/Cl and an additional small amount of HMG (less than or equal to 300 IU). Method III is the combined therapy with Brc/Cl and an increased amount of HMG (less than or equal to 1,200 IU) and HCG. The ovulation rate of method I was 57.5% (23/40) in 40 cases, and 55.6% (99/178) in 178 cycles. The pregnancy rate for this method was 23.8% (5/21). Out of the 12 nonrespondent method I cases, 5 additional cases were ovulated by method II and 3 cases were ovulated by method III. The total pregnancy rate was 42.9% (9/21) with these three methods. Seven cases were normal pregnancies, one case was a twin pregnancy and 1 case was an abortion. No other side effects were found in this study. From these results, the combined therapy with Brc/Cl or Brc/Cl + HMG had almost the same ovulatory rate as the HMG-HCG therapy, and fewer side effects.

Adolescent↗