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PubMed1983

Inhibition of lactation by cyclofenil and bromocriptine.

In a double blind controlled study of the inhibition of lactation 13 women received 300 mg of cyclofenil and 11 women 2.5 mg of bromocriptine twice daily for 14 days. Lactation was effectively inhibited by both drugs, but with bromocriptine there was a significantly higher frequency of relapse. The plasma concentration of prolactin, which decreased rapidly with bromocriptine, returned to the pretreatment level the day after drug treatment stopped, but with cyclofenil it remained low. Plasma oestradiol followed a similar pattern. Plasma FSH increased more rapidly with bromocriptine than with cyclofenil. There was no significant difference between the treatment groups at any stage for haematology, coagulation or liver function tests. The more sustained effect of cyclofenil on prolactin secretion with a reduced frequency of relapse, and the lower oestradiol level, which might indicate a reduced risk of thromboembolism, suggest that this drug has some advantage over bromocriptine in the inhibition of postpartum lactation.

Bromocriptine↗
PubMed1984

Differential effects of bromocriptine on dopamine and acetylcholine release modulatory receptors.

Rabbit neostriatal slices were prelabeled with [3H]dopamine (DA) and [14C]choline and then superfused. The electrical stimulation-evoked release of DA and of acetylcholine (ACh) was abolished by 0.33 microM tetrodotoxin and by low calcium concentrations (0.13 mM). Bromocriptine, a selective D2-DA receptor agonist, inhibited in a concentration-dependent manner the evoked overflow of DA and ACh, without affecting the basal efflux of both transmitters. The effects of bromocriptine were antagonized by sulpiride, a specific antagonist of D2-DA receptors. With stimulation at 0.3 Hz and 120 pulses, bromocriptine was eight times more potent in inhibiting the evoked overflow of DA (IC50: 11 nM) than that of ACh (IC50: 83 nM). Stimulations at 3 Hz and 360 pulses markedly reduced the potency of bromocriptine in inhibiting DA and ACh release, and diminished its selectivity for presynaptic receptors. These results indicate that DA receptors that modulate the release of DA and ACh are of the D2 subtype. The greater potency of bromocriptine at pre- than at postsynaptic sites suggests that these receptors may be different in quantity and/or quality [D2-alpha (presynaptic) versus D2-beta (postsynaptic)]. Finally, marked differences in the potency and efficacy of DA agonist actions on DA and ACh release modulatory receptors are obtained, depending on the parameters of stimulation used.

Acetylcholine↗
PubMed1998

Hypotensive action of bromocriptine in the DOCA-salt hypertensive rat: contribution of spinal dopamine receptors.

To assess the role of spinal dopamine receptors in mediation of hypotension induced by systemic administration of the dopamine D2 receptor agonist, bromocriptine, conscious deoxycorticosterone acetate (DOCA)-salt hypertensive rats were pretreated with either intravenous (i.v.; 500 micrograms/kg) or intrathecal (i.t.; 40 micrograms/rat at T9-T10) domperidone, a selective dopamine D2 receptor antagonist that does not cross the blood-brain barrier. In DOCA-salt hypertensive rats, i.v. administration of a sub-maximal dose of bromocriptine (150 micrograms/kg) induced a significant decrease in mean aortic pressure (MAP) which was greater and longer lasting than that in uninephrectomized control rats. Intravenous or i.t. pretreatment with domperidone reduced partially, but significantly, the hypotensive effect of bromocriptine (reduction of about 57% and 45% of the maximal effect, respectively). The remaining responses observed during the 60 min postinjection period were still statistically significant as compared with vehicle injection. In contrast, the bromocriptine-induced hypotension was fully abolished by i.v. pretreatment with metoclopramide (300 micrograms/kg), a dopamine D2 receptor antagonist that crosses the blood-brain barrier, or by combined pretreatment with i.v. and i.t. domperidone. These results suggest that, in DOCA-salt hypertensive rats, the hypotension induced by i.v. bromocriptine is mediated partly through a peripheral D2 dopaminergic mechanism and partly through stimulation of spinal dopamine D2 receptors, has been demonstrated in conscious normotensive rats.

Animals↗
PubMed1984

Effects of dopamine and bromocriptine on colonic motility in dog.

The effects of intravenous infusions of dopamine (0.1 to 1 mg kg-1h-1) and bromocriptine (10 to 40 micrograms kg-1h-1) on colonic motility were investigated in fasted dogs fitted with permanent strain gauges on the ascending, transverse and descending colon. Infused at rates of 0.5 and 1 mg kg-1h-1 during 1 h, dopamine immediately stimulated the motility of the descending colon; after a delay of 40 to 60 min this effect was balanced by an inhibition of the motility of the ascending and transverse colon. Bromocriptine infused intravenously at doses of 10 to 40 micrograms kg-1h-1 stimulated the motility of the whole colon but these effects were limited to the duration of the infusion (60 min). Both propranolol (0.5 mg kg-1) and tolazoline (2 mg kg-1) failed to block the effects of dopamine and bromocriptine whereas phentolamine (0.1 mg kg-1) and prazosin (0.2 mg kg-1) partially reduced the inhibitory effects of dopamine on the proximal colon. Haloperidol at doses higher than 0.2 mg kg-1 and domperidone blocked the bromocriptine-induced stimulation of colonic motility which was unaffected by previous treatment with alpha- and beta-adrenoceptor blocking agents. These results suggest that in the dog, dopamine and bromocriptine stimulate colonic motility through specific dopamine receptors. However, they suggest that the inhibitory effects of dopamine on the proximal colon which are blocked by dopamine antagonists are also partially due to an effect on alpha 1-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1981

Bromocriptine and its use in Parkinsonism.

Bromocriptine is a potent dopamine agonist which directly stimulates dopamine receptors. In the corpus striatum, this action results in alleviation of many of the signs and symptoms of parkinsonism. The effectiveness of bromocriptine may persist for at least one to two years; results of more prolonged treatment are not available. Adverse reactions are common and often severe, but safety in dosages up to 100 mg daily for one to two years has been adequately established. Bromocriptine is qualitatively and quantitatively similar to levodopa in both beneficial and adverse effect. However, because of variations in individual response, bromocriptine sometimes ameliorates the problems of prolonged levodopa therapy, i.e., declining efficacy, fluctuations in therapeutic response, and the development of disabling abnormal involuntary movements, Thus bromocriptine is a valuable adjunct in the treatment of parkinsonism.

Antiparkinson Agents↗
PubMed1986

Selective regional effect of various neuroactive drugs on bromocriptine concentration in the brain of rats.

Bromocriptine (2-Br-alpha-ergocryptine), a partial ergoline derivative, is a dopamine agonist which has been used successfully in the treatment of hyperprolactinemia, acromegaly and Parkinson's disease. The main targets for the action of the drug are the hypothalamic, hypophyseal pathway and the striatum. These regions contain different populations of neurons which interact with each other in a complex way. In order to check the mechanism of these interactions in rats, we administered different neuroactive drugs together with bromocriptine. After a single intraperitoneal injection, bromocriptine concentration in the striatum was 13.1 +/- 2.9 ng/mg protein, and in the hypothalamus 13.9 +/- 0.8 ng/mg protein. The largest increase in the bromocriptine content in the striatum was found after the concomitant administration of naloxone, an opiate receptor blocker (21.2 +/- 2.5 ng/mg protein). The largest increase of the bromocriptine content in the hypothalamus was found after the concomitant injection of methysergide, a serotonin receptor blocker (27.8 +/- 2.6 ng/mg protein). Amantadine, diazepam and haloperidol caused the largest decrease in the two regions. The mechanism of interaction and therapeutic implication of these findings are discussed.

Amantadine↗
PubMed1992

Comparison of lisuride and bromocriptine in the treatment of advanced Parkinson's disease.

Twenty patients with advanced idiopathic Parkinson's disease were studied, all having a deteriorating response to levodopa and suffering from daily fluctuations in disability. A double-blind randomized cross-over study was conducted. Basic levodopa and anticholinergic treatment was continued unchanged in all patients. The dose increment period of 4-8 weeks was followed by a 4 week treatment period on a fixed optimal dose. In both treatment groups the mean optimal daily dose of lisuride was 1.3 mg (range 0.2-2.4 mg) and that of bromocriptine about 15 mg (range 3.75-30.0), without any significant differences between the treatment groups. The addition of lisuride or bromocriptine to levodopa treatment resulted in a significant and equal further improvement of parkinsonian disability. The therapeutic profiles of both lisuride and bromocriptine were similar. There was significantly more improvement in tremor than in other parkinsonian symptoms. Both lisuride and bromocriptine elicited a significant improvement in fluctuations of disability. No significant differences between the treatments were observed. The occurrence of clinical side effects seemed to be similar with both treatment regimens. In advanced parkinsonian patients the therapeutic efficacy of lisuride seems to be equal to that of bromocriptine as far as parkinsonian disability and fluctuations in disability are concerned.

Aged↗
PubMed1985

Management of pituitary gigantism. The role of bromocriptine and radiotherapy.

True gigantism with overproduction of growth hormone (GH) and prolactin (PRL) was diagnosed in two boys, aged 13 years (case I) and 7 1/2 years (case II). Both had shown increased growth rates since early childhood (from 4 years and 1 1/2 years, respectively), but no skeletal acromegalic features were noted. However, both showed increased sweating and both had advanced pubic hair relative to testis volume. No other pituitary dysfunction was recorded. Case I underwent transsphenoidal surgery with only incomplete and temporary suppression of GH and PRL levels. However, in both patients bromocriptine administration promptly suppressed PRL levels. Following combined irradiation and bromocriptine treatment, GH also gradually normalized over a period of 2 years. Both boys are still on treatment, and both showed an increase in plasma GH concentrations when the dose of bromocriptine was reduced or discontinued, indicating that even 3 1/2-5 years after irradiation therapy (and during continuous treatment with bromocriptine) the disease was controlled but not cured. However, in these two boys bromocriptine has proved effective in controlling the PRL/GH oversecretion.

Body Height↗
PubMed1979

The effects of bromocriptine on pre-synaptic and post-synaptic alpha-adrenoceptors in the mouse vas deferens.

Noradrenaline (NA) and dopamine (DA) contracted the mouse vas deferens and reduced the responses to low frequency nerve stimulation (0.1 Hz). The relative potencies of antagonists suggested that these effects were due to stimulation of post-synaptic and pre-synaptic alpha-adrenoceptors respectively. Bromocriptine produced a non-competitive antagonism of contractile responses to NA (pD2' = 7.6) and DA (pD2' = 8.0) but had no effect on responses to carbachol. Bromocriptine also reduced single twitch responses of the vas to low frequency field stimulation (0.1 Hz), but did not affect stimulation at higher frequencies (1--20 Hz). Yohimbine selectively and rapidly reversed the inhibiting effects of bromocriptine on single twitches, although they could not easily be reversed by washing. Bromocriptine produced a yohimbine-reversible reduction in the stimulated overflow of tritium from vasa previously loaded with 3H--NA. Thus the mouse vas deferens does not appear to contain specific DA receptors and the results suggest that bromocriptine acts as a pre-synaptic alpha-adrenoceptor agonist and post-synaptic alpha-adrenoceptor antagonist in this tissue.

Animals↗
PubMed1979

Value of bromocriptine in unexplained primary infertility: a double-blind controlled trial.

In a double-blind controlled study, 47 women with unexplained primary infertility were allocated at random to treatment with either bromocriptine 2.5 mg twice daily (24 patients) or placebo (23). Both groups showed a fall in serum prolactin concentrations but the reduction was much greater in the bromocriptine-treated group. Neither group showed a change in serum oestrogen or progesterone concentrations. Bromocriptine significantly reduced the duration of the follicular phase of the menstrual cycle but had no effect on the luteal phase. Five women conceived during treatment with placebo and seven during treatment with bromocriptine, but analysis of the cumulative conception rates showed no significant difference between the groups. The women who conceived were significantly younger and had a significantly shorter history of infertility than the women who did not conceive, but subtracting the number of years of infertility from age eliminated this difference. The results show that bromocriptine in the dose and duration of administration used in the trial is of no value in unexplained primary infertility.

Adult↗
PubMed1983

Failure of bromocriptine to maintain reduction in size of a macroprolactinoma.

A patient with a macroprolactinoma was treated with bromocriptine 15 mg daily. Both the size of the tumour as shown by computed tomography and the serum prolactin concentration decreased over several months but then increased. The dose of bromocriptine was increased to 40 mg daily but tumour growth continued, and the tumour was resected. Production of prolactin by cultured cells was not inhibited by high concentrations of bromocriptine, suggesting that regrowth of the tumour was due to cells resistant to dopamine agonist action. This case of regrowth of a prolactinoma during bromocriptine treatment after an initial reduction in size indicates the need for close surveillance especially of patients whose serum prolactin concentration fails to fall into the normal range with bromocriptine treatment.

Bromocriptine↗
PubMed1978

Treatment of the on-off syndrome in Parkinsonism with low dose bromocriptine in combination with levodopa.

The addition of bromocriptine, given in divided doses up to 30 mg per day, to conventional anti-Parkinsonism therapy has been studied in a double-blind placebo controlled clinical trial in 11 patients with Parkinsonism with the "on-off" syndrome. Four patients withdrew because of side effects. Of the seven remaining, three had clinical benefit from bromocriptine with reduction in severity and frequency of fluctuations. There was, however, no statistically significant benefit of bromocriptine when the group as a whole was assessed in terms of severity or frequency of fluctuations measured by three different methods. The mean frequency of major fluctuations on placebo was 2.9/day and on bromocriptine 1.8/day (P less than 0.1 greater than 0.05). There appears to be a limited role for bromocriptine as additional therapy in the management of some patients with the on-off syndrome.

Antiparkinson Agents↗
PubMed1978

Growth hormone and prolactin response to bromocriptine in patients with Huntington's chorea.

The growth hormone (hGH) and prolactin (hPRL) responses to oral bromocriptine were studied in two groups of patients with Huntington's chorea and in seven healthy control subjects. The patients included six patients who had previously been treated with phenothiazines and six patients who had not received phenothiazine treatment. All medication was stopped 72 hours before the investigation which involved taking blood samples for up to 210 minutes after taking bromocriptine (2.5 mg). Plasma samples were analysed for hGH and hPRL. There was no significant difference in basal hGH concentrations between the patients and control subjects. The hGH response to bromocriptine varied in the individual patients but the concentrations were significantly lower in the patients compared with the controls between 160 and 210 minutes. The basal concentrations of hPRL were also not different, apart from the findings of elevated hPRL concentrations in three patients previously treated with phenothiazines. The patients and control subjects showed a consistent fall in hPRL concentrations after taking bromocriptine. The lower peak hGH response to bromocriptine found in the patients suggests that there may be an alteration of dopaminergic neurones mediating hGH release.

Adult↗
PubMed1979

Long-term treatment of Parkinson's disease with bromocriptine.

BRomocriptine (15-75 mg per day) alone or with L-dopa was studied during five to 29 months on 44 patients with Parkinson's disease. Used as sole therapeutic agent, it was found excellent in 12 patients who had never received regular L-dopa treatment either because it was never attempted or because of intolerance from the outset. Its anti-Parkinsonism activity was comparable with L-dopa. The gain was stable in the long term until this report. The side effects of L-dopa were not seen after bromocriptine. In cases where L-dopa had ceased to be active, bromocriptine produced a further improvement if mental deterioration was not associated. In very advanced forms of Parkinson's disease with associated dementia, bromocriptine did not produce durable results. Bromocriptine did not improve the "on-off" effects but reduced a number of the side effects of L-dopa, in particular cardiac, painful contractions, and dyskinesia without "on-off" effects.

Adult↗
PubMed1981

Bromocriptine therapy in acromegaly. A long-term review of 35 cases.

Bromocriptine (CB-154, Parlodel, Sandoz) was given to 35 acromegalic patients for a period of 6-36 months. Basal and post-therapy endocrine functions including estimation of serum growth hormone (GH) profile; and GH kinetics during oral glucose tolerance test, augmented insulin tolerance test and thyrotrophin releasing hormone test were determined. The pituitary tumour size was delineated by a pneumoencephalogram. The mean GH levels ranged from 14 micrograms/l to 316 micrograms/l. Bromocriptine suppressed GH values to 5 micrograms/l or less in 16 patients and less than 10 micrograms/l in a further 6 patients. In 33 patients GH values fell to 50% of the basal value or less. There was no significant GH reduction in 2 'nonresponders'. Bromocriptine did not block the stress-induced GH secretion. It did not disturb pituitary functions other than prolactin which was suppressed much earlier and was maintained with smaller doses. GH suppression on the other hand was shortlived and rebounded when the drug was omitted. It had no adverse effect on tumour size in 2 patients having suprasellar extension of the tumour. Bromocriptine improved carbohydrate tolerance and sexual function although it did not affect insulin and gonadotrophin values. It seems reasonable to offer a trial of bromocriptine in all patients with acromegaly where therapy is deemed necessary as it is well tolerated, has insignificant side effects and no adverse drug interactions. Its high cost and prolonged course are obvious disadvantages. Caution should be exercised in cases with suprasellar extension and visual field involvement.

Acromegaly↗
PubMed1998

Bromocriptine reduces obesity, glucose intolerance and extracellular monoamine metabolite levels in the ventromedial hypothalamus of Syrian hamsters.

We examined whether reductions in body fat stores and insulin resistance in Syrian hamsters induced by bromocriptine are associated with reductions in daily norepinephrine (NE) and serotonin activities as indicated by their extracellular metabolite levels in the ventromedial hypothalamus (VMH). High levels of these monoamines within the VMH have been suspected to induce obesity and insulin resistance. Microdialysate samples from the VMH of freely moving obese male hamsters (BW: 208 +/- 5 g) were collected hourly over a 25-hour period before bromocriptine treatment, during the first day of and after 2 weeks of bromocriptine treatment (800 microg/animal daily, i.p.), and body composition and glucose tolerance analyses were conducted before and after 2 weeks of treatments. The microdialysate samples were analyzed by HPLC for metabolites of serotonin: 5-hydroxy-indoleacetic acid (5-HIAA), NE: 3-methoxy-4-hydroxy-phenylglycol (MHPG), and dopamine: homovanillic acid (HVA). Bromocriptine treatment for 14 days significantly reduced body fat by 60% and areas under the glucose and insulin curves during a glucose tolerance test by 50 and 46%, respectively. Concurrently, extracellular VMH contents of 5-HIAA, MHPG, and HVA were reduced by 50, 29 and 66%, respectively (p < 0.05). Similarly, VMH 5-HIAA and MHPG contents were 48 and 44% less, respectively (p < 0.05), in naturally glucose-tolerant hamsters compared with naturally glucose-intolerant hamsters. Bromocriptine induced reductions of body fat, and improvements in glucose intolerance may result in part from its ability to decrease serotonin and NE activities in the VMH.

Adipose Tissue↗
PubMed1996

Eight-year follow-up study of bromocriptine monotherapy for Parkinson's disease.

An 8-year nationwide study of bromocriptine monotherapy and combination therapy with bromocriptine and levodopa in Parkinson's disease is reported. Fifteen patients were on bromocriptine monotherapy, and 44 patients on bromocriptine combined with levodopa for a certain time during an 8-year period. By judging from Hoehn and Yahr's grading, 4 of the 15 patients in the monotherapy group were in a better condition than before treatment, while 7 cases remained in the same grading, and only 4 showed deterioration. On the other hand, 26 of 44 patients on combination therapy showed more advanced grading at the end of 8 years compared to the stage at the onset of the trial. Maintenance doses of bromocriptine in the two groups were 12-13 mg per day, and levodopa doses were kept at a relatively low level (310-370 mg per day) during this study period. Whether dopamine receptor agonists have neuroprotective effect or not is extremely difficult to prove in human subjects, but this type of long-term follow-up study might give some clues as to these important questions.

Aged↗
PubMed1994

Seven-year follow-up study of bromocriptine therapy for Parkinson's disease.

A 7-year nationwide study of bromocriptine monotherapy and combination therapy with bromocriptine and levodopa in Parkinson's disease is reported. Of 22 patients who had been on bromocriptine monotherapy for 7 years (group B), 16 remained improved or remained in the same stages of Hoehn and Yahr, and no wearing-off phenomenon or dyskinesia was observed. In another 56 patients who were started on bromocriptine alone, but in whom combination therapy with levodopa was instituted at some time in the 7 years (group BL), disease progressed faster than in group B. A wearing-off phenomenon and dyskinesia occurred in 34% and 5.4% of the patients, respectively. These manifestations appeared only after initiation of levodopa. The favorable course of group B suggests possible neuroprotective effects of bromocriptine or may be due to the inevitable selection of patients who had a favorable course originally.

Adult↗