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PubMed2002

Alterations in striatal neuropeptide mRNA produced by repeated administration of L-DOPA, ropinirole or bromocriptine correlate with dyskinesia induction in MPTP-treated common marmosets.

Chronic administration of L-DOPA to MPTP-treated common marmosets induces marked dyskinesia while repeated administration of equivalent antiparkisonian doses of ropinirole and bromocriptine produces only mild involuntary movements. The occurrence of dyskinesia has been associated with an altered balance between the direct and indirect striatal output pathways. Using in situ hybridisation histochemistry, we now compare the effects of these drug treatments on striatal preproenkephalin-A (PPE-A) and adenosine A(2a) receptor mRNA expression as markers of the indirect pathway and striatal preprotachykinin (PPT) mRNA and preproenkephalin-B (PPE-B, prodynorphin) mRNA expression as markers of the direct pathway.The equivalent marked losses of specific [3H]mazindol binding in the striatum of all drug treatment groups confirmed the identical nature of the nigral cell loss produced by MPTP treatment. MPTP-induced destruction of the nigro-striatal pathway markedly increased the level of PPE-A mRNA in the caudate nucleus and putamen and decreased the levels of PPT and PPE-B mRNA relative to normal animals. Repeated treatment with L-DOPA for 30 days produced marked dyskinesia but had no effect on the MPTP-induced increase in PPE-A mRNA in the caudate nucleus and putamen. In contrast, L-DOPA treatment normalised the MPTP-induced decrease in the level of PPT and PPE-B mRNA. Repeated treatment with ropinirole produced little or no dyskinesia but markedly reversed the MPTP-induced elevation in PPE-A mRNA in the caudate nucleus and putamen. However, it had no effect on the decrease in PPT or PPE-B mRNA. Similarly, bromocriptine treatment which induced only mild dyskinesia attenuated the MPTP-induced elevation in PPE-A mRNA in the caudate nucleus and putamen with no effect on reduced striatal PPT or PPE-B mRNA. Neither MPTP treatment nor treatment with L-DOPA, bromocriptine or ropinirole had any effect on adenosine A(2a) receptor mRNA in the striatum. These patterns of alteration in striatal PPE-A and PPT and PPE-B mRNA produced by L-DOPA, bromocriptine and ropinirole show differential involvement of markers of the direct and indirect striatal output pathways related to improvement of locomotor activity and mirror the relative abilities of the drugs to induce dyskinesia.

Animals↗
PubMed2002

Evidences for involvement of nitric oxide in the gastroprotective effect of bromocriptine and cyclosporin A on water immersion stress-induced gastric lesions.

Previous studies have been shown that the adrenergic system involves in gastric secretion and pathogenesis of peptic lesion and activation of alpha(2)-adrenoceptors located on the vagus nerve inhibits gastric acid secretion. Bromocriptine, a dopamine receptor agonist, also has alpha(2) agonistic effect and prevents indomethacin-induced gastric ulcer. alpha(2)-Adrenoceptors involve in the release of nitric oxide which has cytoprotective activity in gastric mucosa. Cyclosporin A (CsA) has also been suppressed stress-induced gastric mucosal lesions, dose dependently. The object of this study was to clarify the interaction between the anti-ulcer effect of bromocriptine (2, 4, 8 mg kg(-1)) or cyclosporin A (5, 10, 20 mg kg(-1)) and nitric oxide. Intraperitoneal injections of bromocriptine and cyclosporin A prevented water immersion stress-induced gastric ulcer in rats. L-Nitro-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, increased stress-induced lesions while L-arginine, a precursor of nitric oxide, decreased these lesions. In conclusion, increasing level of nitric oxide by bromocriptine and cyclosporin A may be one of the contributory factors in their protective effects on gastric mucosa.

Animals↗
PubMed1981

Method of addition of bromocriptine to the drug regime of patients with advanced Parkinson's disease.

Using a method of a gradual increase of bromocriptine with a concomitant reduction of Sinemet (levodopa 250 mg + carbidopa 25 mg), 19 patients with advanced Parkinson's disease have been treated for periods of up to 22 months and 16 of them have shown improvements of varying degrees. Eighteen patients were able to tolerate bromocriptine addition, with early transient adverse effects occurring in seven cases. In contrast to several previously reported studies, it was found necessary to withdraw bromocriptine in only one case. With the drugs currently available, bromocriptine has a role in the management of patients with advanced Parkinson's disease. The method described here may allow a greater number of patients to be given a trial with this drug.

Aged↗
PubMed1984

Bromocriptine in the management of end of dose deterioration in Parkinson's disease.

Thirty-three patients with advanced Parkinson's disease complicated by end of dose deterioration were treated with bromocriptine. The drug was slowly increased so that by treatment week 24 the mean daily dose of bromocriptine was 22mg and levodopa had been decreased by an average of 15 percent. The majority of improvement in daily fluctuations and Parkinsonian disability score was documented by 8 weeks, at which time the mean daily bromocriptine dose was only 12mg. End of dose deterioration was reduced in 78 percent of the patients (mean 43% improvement). Total Parkinsonian disability score was decreased by 33 percent. Adverse effects were minimal; the most common was mild transient early treatment nausea which occurred in 15 percent of the patients. The slow introduction of small doses of bromocriptine, combined with minimal levodopa reduction, can give Parkinsonian patients significant improvement in end of dose deterioration.

Adult↗
PubMed2000

Bromocriptine markedly suppresses levodopa-induced abnormal increase of dopamine turnover in the parkinsonian striatum.

Bromocriptine, a dopamine agonist, is commonly used in combination with levodopa for the treatment of Parkinson's disease (PD). To investigate the theoretical basis of such combination therapy, we examined the effects of bromocriptine administered alone or in combination with levodopa on dopamine turnover in the striatum of hemi-parkinsonism rats. The parkinsonian striatum showed a 3.4-fold increase of dopamine turnover relative to the control striatum, as often observed in the brain of PD patients. A 7-day course of levodopa therapy markedly increased dopamine turnover in the parkinsonian striatum (53-fold of control level) than in the control striatum (5-fold of the control level). However, bromocriptine specifically and markedly suppressed the levodopa-induced abnormal activation of dopamine turnover in the parkinsonian striatum. Our findings explain the pharmacological basis for the introduction of bromocriptine during long-term levodopa therapy.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

Piribedil and bromocriptine in Parkinson's disease: a single-blind crossover study.

INTRODUCTION: Clinicians switch from one dopamine agonist to another for various reasons. However, each change may inadvertently result in certain potential risks such as decreased medication efficacy or new side-effects. OBJECTIVE: We evaluated the tolerability of a switch of bromocriptine to piribedil using two conversion ratios as a primary outcome measure, with motor function as a secondary outcome measure, in patients with mild to moderate Parkinson's disease (PD). METHODS: Twenty consecutive patients with mild to moderate PD (Hoehn and Yahr, stage II-III) on treatment with stable doses of bromocriptine and levodopa were randomized to two groups of 10 patients each, to receive piribedil based on 1:5 or 1:10 conversion ratios. Blinded evaluations were performed: 1) United Parkinson's Diseased Rating Scale (UPDRS) scores both in 'on' and 'off', 2) Open-ended interviews for adverse events, 3) Epworth Sleepiness Scale, 4) Purdue Pegboard assessment during 'on' and 'off', 5) Hand-arm movement test during 'on' and 'off', and 6) Walking test during 'on' and 'off'. RESULTS: Major adverse events included 'sleep attacks' in one patient and minor side-effects included giddiness, nausea, hallucinations, sleepiness and lethargy. However, these were mild and 19 (95%) of the 20 patients completed the study. There was a significant improvement in both the UPDRS 'off' total and motor scores at 1 month compared with baseline for the group on 1:10 ratio. The walking times during the 'off' state at 1 and 2 months were significantly better compared with baseline in the 1:5 group. There were otherwise no significant differences in the rating tests during both 'off' and 'on' states before and after the bromocriptine switch. CONCLUSIONS: We demonstrated that patients with mild to moderate PD who were on relatively low doses of bromocriptine can be safely switched to piribedil based on a conversion ratio of either 1:5 or 1:10. However, the higher conversion ratio has to be carried out with caution in patients with daytime somnolence.

Administration, Oral↗
PubMed2001

Effects of chronic bromocriptine treatment on tyrosine hydroxylase (TH) mRNA expression, TH activity and median eminence dopamine concentrations in ageing rats.

The purpose of this study was to investigate the age-related changes in the responsiveness of tuberoinfundibular dopamine (TIDA) neurones to chronic hypoprolactinemia induced by treatment with bromocriptine, a dopamine receptor agonist. In one experiment, TIDA neuronal activity after acute hypoprolactinemia or exogenous prolactin was monitored by measuring tyrosine hydroxylase (TH) activity in the stalk median eminence of middle-aged cycling female rats (10-12 months), old constant oestrous rats (18-20 months) and old pseudopregnant rats (22-24 months). In another experiment, middle-aged cycling (10-12 months) rats were treated with bromocriptine for 6 or 12 months. TH activity was measured in the stalk median eminence, TH mRNA levels were measured in the arcuate nucleus and dopamine concentrations were measured in the arcuate nucleus and median eminence. Responsiveness of TIDA neurones to exogenous prolactin and to the withdrawal of bromocriptine in these rats was also tested. While the TIDA neurones in all three age groups responded to acute hypoprolactinemia by showing a reduction in TH activity, older rats failed to respond to exogenous prolactin administration. In contrast, chronic hypoprolactinemia for 12 months enabled the rats to retain TIDA neuronal responsiveness to exogenous prolactin. It also decreased TIDA neuronal function as measured by dopamine concentrations in the median eminence, TH activity in the stalk median eminence and TH mRNA in the arcuate nucleus of ageing rats. The restoration of the responsiveness of these neurones to prolactin stimulation in older rats demonstrates for the first time that hypoprolactinemia produced by chronic bromocriptine treatment indeed provides a neuroprotective effect on TIDA neurones. These results indicate that maintaining a low level of neuronal activity by lowering prolactin levels may be a contributing factor in retaining the plasticity of TIDA neurones.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Use of bromocriptine to prevent puerperal lactation during neuroleptic treatment of chronic schizophrenia.

Bromocriptine, the ergotamine alkaloid 2-bromo-alpha-ergocriptine, is known as a dopamine D-2 receptor agonist with strong prolactin-lowering actions and potential mental side-effects. The case reported here involves a female chronic schizophrenic patient in childbed who was treated both with neuroleptics and with bromocriptine; the latter was given in order to prevent inappropriate puerperal lactation. The described therapeutic regimen succeeded in preventing puerperal lactation without exacerbating schizophrenic symptoms. The simultaneous use of neuroleptics and bromocriptine was accompanied by monitoring for changes in mental status and plasma prolactin level. The high prolactin plasma levels that persisted in spite of treatment with bromocriptine would seem to be a reason to carry out further research into the mechanism of action of the drug.

Adult↗
PubMed1980

[Effect of high single doses of bromocriptine in schizophrenic patients with elevated serum prolactin levels and extrapyramidal side effects associated with neuroleptic treatment (author's transl)].

The purpose of the present study was to investigate the effect of bromocriptine in single doses of 20 and 30 mg on the unwanted effects most frequently caused by neuroleptics: elevated prolactin levels and extrapyramidal disturbances. 111 chronic schizophrenics were included in the investigations, 58 of them being treated with haloperidol and 53 with chlorpromazine. It was found that a single dose of 30 mg bromocriptine brought about a statistically significant decrease in the prolactin levels of patients treated with haloperidol but produced no more than a downward tendency in patients receiving chlorpromazine (the initial prolactin levels of both groups of patients were equal.) The effect of bromocriptine on EPS disturbances was more marked in the chlorpromazine group, but side effects such as nausea and agitation also occurred more frequently in this group. These results show that there is no correlation between the reduction in prolactin levels produced by bromocriptine and an improvement in unwanted EPS effects. This supports the hypothesis that the effect of neuroleptics on the prolactin secreting cells of the anterior pituitary and their effect on the EPS are mediated by different sets of receptors.

Adult↗
PubMed1989

[Bromocriptine: a new therapy concept in the treatment of chronic recurrent uveitis?].

Chronic recurrent uveitis still responds unsatisfactorily to therapy. Prolactin, a pituitary hormone that attains high blood levels physiologically in stress situations, has an immune modulating effect. The prolactin antagonist bromocriptine (2 x 2.5 mg/day) was administered prophylactically to prevent recurrence in seven patients with chronic iritis/iridocyclitis or panuveitis (Group A). On this therapy two patients suffered a mild recurrence (in one case in the first month). Another patient developed rebound uveitis after discontinuing bromocriptine medication. Tolerance appears to vary considerably, and in three patients the therapy had to be discontinued because of arterial hypotension and congestive rhinopathy, respectively. The three patients in Group B (with iritis, sympathetic ophthalmia, and intermediate uveitis) received bromocriptine in addition to cyclosporin A after plasmapheresis. This combination resulted in an elevated cyclosporin A plasma level, and the dosage was reduced by 30-50% (plasma level 70-120 ng/ml). With this lower dosage of cyclosporin A, the creatinine level of one of the patients returned to normal. Viewed on the basis of these initial results bromocriptine would appear to reduce the number of recurrences of chronic uveitis. Moreover, the synergism with cyclosporin A, described both theoretically and in an animal model in the literature, appears attainable in therapy.

Adult↗
PubMed1981

[Bromocriptine induced cystic tumour regression in advanced prolactinomas (author's transl)].

Conservative treatment with bromocriptine was performed in three patients with macroprolactinomas and increased prolactin levels. Lowering of prolactin levels to normal or subnormal values was possible in all cases. One extensive prolactinoma with retro- and suprasellar parts showed regression to a large extent and cystic degeneration. Transient occurrence of liquorrhoea is considered as a consequence of tumour regression. In cases of parasellar prolactinoma recurrence and intrasellar prolactinoma diminution and cystic degeneration were observed while on bromocriptine treatment. Bromocriptine dosage varied between 3.75 and 30 mg/d. Treatment was performed between 20 and 26 months. There were no serious side effects. Bromocriptine treatment offers an alternative to surgery in macroprolactinomas and prolactinoma recurrences.

Adult↗
PubMed1976

Treatment of parkinson's disease with bromocriptine.

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P less than 0.01) improvement in rigidity, tremor, bradykinesia, gait disturbance and total score. In seven patients levodopa with carbidopa was completely replaced by bromocriptine (mean dose, 70 mg), with improvement in four. Adverse effects were similar to those observed with levodopa and carbidopa, except that in individual patients abnormal involuntary movements and diurnal oscillations in performance (on-off effect) were decreased whereas orthostatic hypotension and mental changes were increased. Bromocriptine appears to be a major new agent in Parkinson's disease that is especially promising in patients no longer responding to levodopa.

Aged↗
PubMed1981

No effect of bromocriptine in acromegaly: a controlled trial.

Although bromocriptine, a dopamine receptor agonist, is now widely used in the treatment of acromegaly, there have been no controlled trials of its biochemical or clinical effects on this disorder. We assessed its effects in a double-blind, crossover study. Eighteen patients with acromegaly were given bromocriptine and placebo alternately for three months per medication. Their responses to oral glucose-tolerance tests during the two regimens did not differ significantly. The number of patients noting amelioration of clinical symptoms during treatment with bromocriptine was almost identical to the number with clinical improvement during placebo. We conclude that it remains doubtful whether bromocriptine has a beneficial effect in acromegaly.

Acromegaly↗
PubMed2005

Rapid re-enlargement of a macroprolactinoma after initial shrinkage in a young woman treated with bromocriptine.

We report the case of a macroprolactinoma in a 32-year-old woman, who presented with secondary amenorrhea, galactorrhea, increased plasma prolactin level (3259 ng/ml), headache and bi-temporal visual field defect. Magnetic resonance imaging showed a large pituitary tumor. The patient responded well to bromocriptine (7.5 mg/day) with improvement of clinical symptoms and normalization of plasma prolactin within a few weeks. After 4 months of treatment, tumor size was also reduced markedly. During continued treatment at the same dose of bromocriptine the plasma prolactin level remained normal, but after 8 months of treatment the patient suddenly complained of worsening of her visual fields, and magnetic resonance imaging indicated re-enlargement of the tumor. Bromocriptine was discontinued and transsphenoidal pituitary surgery was performed. After surgery the visual field defect improved, but postoperative plasma prolactin level (1104 ng/ml) and magnetic resonance imaging indicated a residual tumor. Postoperative treatment with quinagolide (0.15 mg/day) resulted in disappearance of all clinical symptoms, normalization of prolactin level and a reduction in size of the residual tumor. This case demonstrates that a dissociation of the inhibitory effect of bromocriptine on tumor size and prolactin level may rarely develop during the course of drug treatment in a patient with macroprolactinoma.

Adult↗
PubMed1981

Reduction in vulnerability to ventricular fibrillation by bromocriptine, a dopamine agonist.

The effect of a dopamine agonist, bromocriptine, on ventricular fibrillation (VF) threshold was studied in anaesthetised dogs. Bromocriptine produced an increase of 50% in VFT. Pretreatment with the dopamine antagonist haloperidol abolished the effects of bromocriptine on VF threshold as did pretreatment with the peripheral dopamine antagonist, domperidone. It is concluded that bromocriptine reduces vulnerability of the nonischaemic canine ventricle to fibrillation. This effect is most probably mediated by peripheral presynaptic stimulation of dopaminergic receptors, thereby inhibiting noradrenaline release.

Animals↗
PubMed1998

Neuroprotection by bromocriptine against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity in mice.

Mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 30 mg/kg i.p. twice, 16 h apart). This resulted in changes in motor performance and toxic insult of nigral neurons as evidenced by dopamine depletion in nucleus caudatus putamen. In vitro and in vivo treatment of MPTP caused the generation of hydroxyl radicals (.OH) as measured by a sensitive salicylate hydroxylation procedure. A dopamine agonist, bromocriptine (10 microM and 10 mg/kg i.p.), blocked .OH formation caused by MPTP in vitro (20 microM) and in vivo (30 mg/kg i.p.). An MPTP-induced increase in the activity of catalase and superoxide dismutase in substantia nigra on the seventh day was reduced by bromocriptine pretreatment. Bromocriptine blocked MPTP-induced behavioral dysfunction as well as glutathione and dopamine depletion, indicating its potent neuroprotective action. This study suggests that bromocriptine stimulates antioxidant mechanisms in the brain and acts as a free radical scavenger in addition to its action at dopamine receptors, thus indicating its strength as a valuable neuroprotectant.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1998

Acute coronary artery thrombosis in a postpartum woman receiving bromocriptine.

A 35-year-old postpartum woman who was receiving bromocriptine (Parlodel) for only several days to suppress lactation experienced an episode of a seizure, complained of chest pains, and died in the emergency department. At autopsy, acute coronary thrombosis of the left main, left anterior descending, and circumflex arteries was found. Cases of reported cardiac-related complications associated with bromocriptine use in the puerperium are extremely rare. The mechanism of bromocriptine-related acute coronary thrombosis is poorly understood and warrants further scrutiny, because the synthetic brominated ergopeptide is generally regarded as safe. The updated review of reports available in literature mandates the acknowledgment of possible serious and even lethal cardiac events as a result of untoward effects of bromocriptine.

Adult↗
PubMedDate not supplied

MR volumetry for monitoring intramuscular bromocriptine treatment in macroprolactinomas.

OBJECTIVE: To assess volumetric changes of pituitary prolactinomas, we applied a threshold-based segmentation algorithm in two patients during intramuscular bromocriptine treatment. MATERIALS AND METHODS: Tumor volumes were calculated from contiguous slices of a 3D GE sequence and from conventional SE images. RESULTS: After a single 50 mg i.m. bromocriptine administration, the prolactinoma volumes decreased by 25 and 35% within 7 and 11 days, respectively. Volume calculations from 3D GE images were more accurate than calculations from 3 mm 2D SE images, especially for smaller tumors. A decrease of prolactinoma size was paralleled by a decrease of serum prolactin levels and correlated with an improvement of visual field and endocrine function in both patients. The end of the bromocriptine effect was indicated by a reincreasing tumor volume, which was observed after 30 days in the first patients and after 43 days in the second patient. CONCLUSION: Our results suggest that MR volumetry represents a useful tool to monitor changes of prolactinoma volume during bromocriptine treatment and may improve the clinical management of these patients.

Adult↗