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PubMed1987

Hemodynamics, prolactin and catecholamine levels during hemorrhagic shock in dogs pretreated with a prolactin inhibitor (bromocriptine).

Bromocriptin, a dopaminomimetic drug, causing inhibition of prolactin secretion, was used in experiments on haemorrhagic shock in dogs. 5 dogs were treated with bromocriptine (0.4 mg.day-1) for two days; a further 5 dogs were used as control animals. 30% of the blood volume was drawn from each dog. Mean arterial blood pressure, heart rate, central venous pressure, acid-base status, prolactin, GH and catecholamine levels were checked before blood letting and monitored until 1 hour after blood letting. Animals treated with bromocriptine showed a significant decrease of the mean arterial blood pressure and of the prolactin rate and a significant increase of catecholamine levels. Control animals, instead, showed a significant increase of the prolactine and catecholamine rates. The results obtained suggest that bromocriptine can constitute an additional hypotensive factor in subjects with acute haemorrhage. A considerable amount of research work previously carried out has shown a close correlation between stress and hyper-prolactinemia. The increase of prolactinemia and the effects of bromocriptine on this hormone during surgical stress is particularly interesting due to its possible implications (Lanza V. et coll., 1983). In previous experiments involving animals it was found that Prolactin exerts positive chronotropic and hypertensive effects (Horrobin D.F., 1977) whilst bromocriptine is a potent agonist of D2 dopaminergic receptors (Thorner M.O. et coll., 1980). Dopamine was found to be particularly useful in the clinical treatment of shock thus suggesting an involvement of peripheral D2 receptors. On the basis of these observations we have considered it worthwhile to investigate the haemodynamic effects of bromocriptine in haemorrhagic shock.

Animals↗
PubMed1985

Effect of bromocriptine on prostacyclin release and cyclic nucleotides on rat aortic and uterine tissues.

The effect of bromocriptine mesylate on cyclic nucleotides and PGI2 release by rat aortic and uterine tissues was investigated. Treatment of rats with bromocriptine (10 mg kg-1 I.P. daily for 14 days) increased PGI2 release by the thoracic aorta from 0.67 +/- 0.02 to 1.4 +/- 0.03 ng/mg wet tissue (P less than 0.001; n = 6). This increase was antagonized by treatment with sulpiride (15 mg kg-l). Incubation of the arterial tissue with bromocriptine (50 micrograms ml-1) in vitro also stimulated PGI2 release. Mepacrine (160 micrograms ml-1) significantly decreased both basal and stimulated PGI2 release. Incubation of myometrial tissue from pregnant rats with bromocriptine (50 micrograms ml-1) in vitro significantly decreased PGI2 release from 1.25 +/- 0.07 to 0.60 +/- 0.08 ng/mg wet tissue (P less than 0.05, n = 6). It also elevated uterine cAMP from 40 +/- 2 to 64 +/- 3 pmoles/100 mg wet tissue. Both effects were antagonized by sulpiride. Bromocriptine did not affect uterine cGMP or the cyclic nucleotides in the aorta. It is concluded that the increase in aortic PGI2 was mediated via activation of dopamine D-2 receptors that stimulate phospholipase A2 enzyme. The decrease in myometrial PGI2 release may be related to the increase in uterine cAMP resulting from activation of dopamine D-1 receptors. Previous studies suggested a role for PGI2 in implantation in the rat. The results suggest that the inhibitory effect on uterine PGI2 may underlie the reported inhibition of bromocriptine on implantation. On broad basis, the decrease in uterine PGI2 together with the reported luteolytic effect of bromocriptine point to a potential role for the compound in postcoital contraception.

Animals↗
PubMed1984

Low dose bromocriptine: a study of acute effects in chronic mediated schizophrenics.

An acute low oral dose (2 mg) of bromocriptine was administered in a randomized double blind fashion to 11 chronic symptomatic mediated schizophrenic patients. There was an overall improvement for the group on the Brief Psychiatric Rating Scale (BPRS) following bromocriptine. Plasma homovanillic acid, 3-methoxy-4-hydroxyphenylglycol, and vanilloyl-mandelic acid concentrations were unchanged after bromocriptine. Bromocriptine concentrations in the plasma showed a large inter-individual variation. There was a significant inverse correlation between plasma bromocriptine concentration and total BPRS score at 60 minutes post-bromocriptine administration. These results suggest a need for further replication in a larger study population and a need for controlled studies with chronic administration of low dose bromocriptine in chronic medicated schizophrenic patients.

Adult↗
PubMed2006

Bromocriptine reduces steatosis in obese rodent models.

BACKGROUND/AIMS: Obesity is a risk factor for glucose intolerance, steatosis, and oxidative stress, characteristics of nonalcoholic fatty liver disease. Bromocriptine may have anti-obesity, insulin-sensitizing, lipolytic, and antioxidant properties. We, therefore, hypothesized that bromocriptine would improve markers of nonalcoholic fatty liver disease in obese rodent models. METHODS: We performed a randomized, controlled experiment in genetically obese fatty Zucker rats and diet-induced obese rats to assess for behavioral and peripheral anti-obesity actions of bromocriptine (10mg/kg) that would improve nonalcoholic fatty liver disease. RESULTS: Behaviorally, food intake decreased and locomotor activity increased in bromocriptine-treated fatty Zucker and dietary-induced obese rats. Peripherally, liver triglycerides were significantly reduced and hepatic manganese superoxide dismutase significantly increased in bromocriptine-treated fatty Zucker and diet-induced obese rats compared to controls. Blood glucose was significantly lower in bromocriptine-treated Zucker rats compared to fatty controls and was no different than that of lean controls. CONCLUSIONS: Improvements in obesigenic behaviors, glucose tolerance, hepatic lipid accumulation, and mitochondrial oxidative stress observed in genetically obese and diet-induced obese rodents indicate that bromocriptine may be promising as a broad-based therapy for nonalcoholic fatty liver disease.

Animals↗
PubMed1989

Effectiveness of vaginal bromocriptine in treating women with hyperprolactinemia.

Treatment of hyperprolactinemia with oral bromocriptine has been associated with a high incidence of side effects. The authors recently demonstrated that, in normal women, the vaginal route of administration was an effective and safe alternative to oral bromocriptine. To evaluate the effectiveness of vaginal bromocriptine in treating women with hyperprolactinemia, the authors treated 15 hyperprolactinemic women with daily vaginal administration of 2.5 mg tablets of bromocriptine. Serum prolactin (PRL) levels and vital signs were measured daily for 6 days, then weekly for 4 weeks. Gastrointestinal side effects were limited to a single episode of mild nausea, and two cases of transient constipation. In all patients there was a dramatic initial reduction in PRL in response to a single 2.5 mg dose of bromocriptine. In 13 patients PRL levels were maintained within the normal range with daily administration of 2.5 mg, whereas in two patients, PRL levels remained higher than normal despite an increase in bromocriptine dose to 5 mg. These results suggest that short term use of vaginal bromocriptine is a safe and effective method of therapy for hyperprolactinemia.

Administration, Intravaginal↗
PubMed1983

Effects of bromocriptine and dopamine on the binding of estradiol to its uterine cytoplasmic receptors.

The in vivo and in vitro effects of bromocriptine on the binding of estradiol 17 beta to its specific uterine receptors were studied in both mature and immature rats. A single i.p. injection of bromocriptine reduced the specific estradiol-receptor interaction in adult rats, while it resulted ineffective in prepubertal animals. The effect of bromocriptine in mature rats was dose-dependent and evident only when using a dose of at least 0.70 mg/kg. Experiments in vitro also showed that in mature rats bromocriptine affected the estradiol-receptor interaction inducing a decrease in binding, which is well correlated to the concentration used. On the contrary, no effect of bromocriptine in vitro was observed when using cytosol obtained from uteri of immature rats. Very similar results were obtained in experiments in vitro when using dopamine instead of bromocriptine. Our results suggest that apparently there are two forms of estrogen receptors, one present both in prepubertal and pubertal age and the other present only in mature animals. The latter is the type of receptor sensitive to both bromocriptine and dopamine and presumably develops under the control of hormonal factors, which are only present at puberty.

Animals↗
PubMed1997

Bromocriptine enhances feeding behavior without changing dopamine metabolism.

Bromocriptine is an ergot derivative and has been thought to act as a selective D2 receptor agonist, but its effects on dopamine release in vivo have not been confirmed. We administered bromocriptine into the striatum of rats and studied the effects on feeding behavior and dopamine release. Bromocriptine was perfused via a microdialysis probe into the ventrolateral striatum of rats fasted for 22 h, and the rats were then allowed to feed freely for 6 h. Bromocriptine perfusion increased food intake in a dose-dependent manner, whereas the extracellular concentrations of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) did not change. Perfusion of (-) sulpiride, a selective D2 receptor antagonist, decreased food intake, but increased dopamine release and the levels of DOPAC and HVA. Pretreatment with (-)sulpiride perfusion for 1 h prior to bromocriptine perfusion inhibited the increase of food intake induced by bromocriptine, and it increased dopamine release and the levels of DOPAC and HVA. These findings suggest that bromocriptine directly perfused into the ventrolateral striatum acts selectively on postsynaptic D2 receptors and enhances feeding behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2003

Low doses of bromocriptine shorten the interestrous interval in the bitch without lowering plasma prolactin concentration.

In order to investigate the effect of different doses of bromocriptine on plasma prolactin concentration and the interestrous interval, beagle bitches were treated twice daily with 5 microg (5-group), 20 microg (20-group), or 50 microg (50-group) bromocriptine per kg body weight orally, starting 28 days after ovulation. In the 5-group, the difference between the mean plasma prolactin concentration before and that during bromocriptine treatment was not significant. In contrast, mean plasma prolactin concentration decreased significantly after the start of bromocriptine treatment in the 20- and 50-groups. The mean interestrous interval was significantly shorter in all three groups than in untreated bitches in the same colony. The mean interestrous interval in the 20-group and that in the 50-group were similar, but both were significantly shorter than that in the 5-group. The results of this study indicate that bromocriptine shortens the interestrous interval in the bitch even when the dose is so low that it does not lower plasma prolactin concentration. Induction of estrus in the bitch by bromocriptine therefore involves a mechanism other than via the lowering of plasma prolactin concentration. Furthermore, this study shows that the extent of shortening of the interestrous interval by bromocriptine is dose dependent.

Animals↗
PubMed1978

Long-term treatment of parkinsonism with bromocriptine.

92 patients with parkinsonism have been treated with bromocriptine for up to 30 months. 48 continue to receive bromocriptine with benefit; of these, 35 take bromocriptine (mean dose 53 mg daily) in combination with levodopa and 13 take bromocriptine (mean dose 45 mg daily) without levodopa. In those who were originally on levodopa, addition of bromocriptine allowed a mean 41% reduction in the dose of levodopa; the largest group of patients to benefit from bromocriptine entered the study because of excessive dyskinesia or "on-off" phenomena induced by levodopa. In 40 patients bromocriptine was stopped because of adverse reactions, absence of therapeutic response, or non-compliance with the protocol. The main problems were psychiatric disturbance (8 patients) and erythromelalgia (7 patients); these effects tended to occur late (mean 6 months and 10 months, respectively) and with high dosage (mean 66 mg and 115 mg daily). Other frequent adverse effects were dizziness and nausea; these began considerably earlier (at 2 months and 1 month) and with much lower dosage (31 mg and 12 mg daily). 4 patients died, for reasons apparently unrelated to therapy.

Bromocriptine↗
PubMed1991

Effects of bromocriptine on experimental GH3 cell tumors.

Bromocriptine in concentrations up to 10(-4) M was studied for morphological and endocrinological effects upon the GH3 cell line as well as the GH1 and AtT-20 cell lines. The cells (10(5)/ml) were incubated with RPMI 1640 or in some experiments Dulbecco's Modified Eagle's Medium supplemented with 10% FCS. Bromocriptine was added in concentrations of 10(-4) to 10(-8) mol/L and aliquots of medium were obtained at 2 and 24 hs for the determination of growth hormone and prolactin. Significant reductions in concentrations of growth hormone and prolactin as well as cell number were observed with a concentration of bromocriptine of 10(-4) M at 24 hs. The electron microscopic appearance of GH3 cells treated with 10(-4) mol/L concentrations of bromocriptine for 24 hs demonstrated extensive and marked vacuolization in the cytoplasm which had already appeared 2 hs after treatment with bromocriptine. In bromocriptine-treated (10(-4) mol/L for 24 hs) GH1 cells and AtT-20 cells, the morphologic features were essentially unchanged, compared to the untreated group. Since many previous reports demonstrated a defective dopamine receptor system in GH3 cells, it must be concluded that bromocriptine has an extradopaminergic action which is selectively observed in GH3 cell.

Animals↗
PubMed1987

Bromocriptine and the clinical spectrum of Parkinson's disease.

As the direct agonist with the widest clinical use, bromocriptine provides a unique window into the clinical spectrum of Parkinson's disease. The efficacy of bromocriptine for therapy of de novo Parkinson's disease has recently been confirmed using a double-blind design with L-Dopa (Sinemet). Over a period of 5.5 months, bromocriptine was found to be as effective as L-Dopa in reducing the functional and neurological disability of Parkinson's disease. This study complements others and demonstrates a role for bromocriptine as de novo therapy. A longitudinal study comparing bromocriptine with L-Dopa is underway, but previous observations with bromocriptine suggest modest, transient beneficial effects with significantly less fluctuation of disability and less dyskinesia when used alone or in combination with L-Dopa. The transient benefits of bromocriptine on progressive disability suggest that both pre- and post-synaptic defects are eventually involved in Parkinson's disease. While agonists with improved efficacy and minimal side effects are required for symptomatic treatment of Parkinson's disease, strategies to protect pre- and post-synaptic neuron populations against progressive dysfunction must be developed.

Aged↗
PubMed1984

Should dopamine agonists be given early or late? A review of nine years experience with bromocriptine.

Experience with bromocriptine in 106 patients treated over nine years was reviewed. Most of the patients were already being treated with levodopa (combined with a peripheral decarboxylase inhibitor). These patients, after having initially achieved a good response to levodopa, were no longer responding satisfactorily. Most of the patients were also experiencing diurnal oscillations in performance: "wearing off" and "on-off" phenomena. In these patients previous attempts at changing the dose (increasing or decreasing) or changing the scheduling of levodopa had been unsuccessful. Bromocriptine was added to levodopa beginning at a dose of 5 mg/day, and each week was increased by another 5 mg/day. At a dose of bromocriptine of at least 25 mg/day, there was a decrease in disability in the majority of patients with a decrease in the severity of the diurnal oscillations in performance (especially "wearing off" phenomena). In most patients, the addition of bromocriptine resulted in an approximately 10% reduction in the dose of levodopa. The majority of patients sustained their improvement at least one year. In some patients improvement was sustained for up to five years. The therapeutic efficacy of bromocriptine was limited in many patients by the occurrence of adverse effects including mental changes, dyskinesias, orthostatic hypotension, and nausea. These adverse effects could often be minimized by reducing the dose of bromocriptine or levodopa. All adverse effects were reversible upon stopping the drug. We have found bromocriptine to be a valuable adjunct in the treatment of these patients.

Aged↗
PubMed1985

Effect of bromocriptine treatment on prolactin, noradrenaline and blood pressure in hypertensive haemodialysis patients.

Bromocriptine (2.5 mg/day orally) produced a significant fall in supine mean arterial pressure in nine hypertensive haemodialysis patients with high serum prolactin levels, without causing significant changes in heart rate. On bromocriptine, there was a significant decrease in the mean value of both serum prolactin and plasma noradrenaline, without significant changes in the mean value of plasma renin activity. A significant relationship was found between the changes in supine plasma noradrenaline and the changes in supine mean arterial pressure induced by bromocriptine. The increase in mean arterial pressure in response to the tilt test was greater on bromocriptine than on placebo although the changes in plasma noradrenaline were reduced by bromocriptine. Similar results were observed during the cold pressor test. These findings suggest that the arterial pressure-lowering effect of bromocriptine is related to the reduction in sympathetic out-flow. The parallel decrease in serum prolactin raises the question of the possible involvement of dopaminergic mechanisms in the development of hypertension in our patients. Moreover, bromocriptine seems to enhance the vascular response to endogenous noradrenaline.

Adult↗
PubMedDate not supplied

Cost-effectiveness of pergolide compared to bromocriptine in the treatment of Parkinson's disease: a decision-analytic model.

OBJECTIVE: To develop a decision-analytic model to assess the cost-effectiveness of pergolide versus bromocriptine in the treatment of Parkinson's disease (PD). METHODS: A Markov decision-analytic model is used to examine cost-effectiveness. The model ran for 20 cycles of 6 months' duration, and the patients progress through six stages: Hoehn-Yahr stages 1-5 and death. The transitional probabilities for each stage are derived from a 12-year longitudinal study of patients with PD. The costs in the model are derived from an expert panel containing six Australian neurologists. A review of the randomized controlled trials comparing the efficacy and safety of pergolide versus bromocriptine was undertaken. Five studies were identified, with four showing that pergolide offers superior efficacy when compared to bromocriptine. The Mizuno et al. (1995) study was the largest of the controlled trials and also measured patient Hoehn-Yahr status before and after treatment. This was identified as the most appropriate source of relative efficacy data for the model. The model examined various scenarios based on alternate durations of superior clinical benefit with pergolide compared to bromocriptine. The main analysis assumed that patients in each arm of the model would have identical Hoehn-Yahr status by the fifth year. Sensitivity analysis was used to determine cost-effectiveness in the case where the therapeutic benefit was of a shorter duration. RESULTS: The Mizuno study indicates that an additional 19.09% of patients improved by at least one stage on pergolide over bromocriptine, with an odds ratio of 2.26 (p < .01). The total health care cost per patient over the 10-year period was $46,323 in the pergolide treatment arm and $47,351 in the bromocriptine treatment arm, an incremental saving of $1028. Patients also spent extra time in Hoehn-Yahr stages 1, 2, and 3. In sensitivity analyses, when the benefit from pergolide expired between 6 months and 5 years after treatment cessation, cost savings ranged from $68 to $2535. CONCLUSION: Pergolide is cost saving and more efficacious than bromocriptine, and is therefore cost-effective.

Antiparkinson Agents↗
PubMed1982

Effect of long term bromocriptine treatment on glucose intolerance in acromegaly.

Blood glucose, plasma GH, insulin and glucagon levels during oral glucose tolerance test before and after treatment with bromocriptine (5-20 mg daily for 2-9 months) were investigated in eleven acromegalic patients with glucose intolerance. Nine out of 11 patients showed improvement or normalization in glucose tolerance after bromocriptine therapy. Basal levels of plasma GH were markedly decreased in 7 of 11 patients treated, although the improved glucose tolerance was not always associated with a drop of basal plasma GH levels. In contrast, basal plasma glucagon level showed a distinct fall in all the patients whose glucose tolerance was improved, but unchanged in whom glucose tolerance was not ameliorated. The mean values of plasma GH and glucagon after oral glucose load were significantly lower during bromocriptine therapy than those before the treatment, respectively. Basal levels of plasma insulin and its response to glucose load did not change after bromocriptine treatment. Bromocriptine thus appears to be a good alternative in the treatment of glucose intolerance in acromegalic patients and the improvement of glucose tolerance by bromocriptine may be related to the reduction in plasma glucagon levels. The possibility, however, is not excluded that a decrease by bromocriptine in the total daily GH secretion is a cause of the improved glucose tolerance.

Acromegaly↗
PubMed1991

Chronic treatment with long-acting bromocriptine does not affect duration of the breeding season, voluntary food intake, body weight, or wool growth in the Scottish blackface ewe.

The aim of this study was to determine whether suppression of the seasonal increase in prolactin concentrations by chronic treatment with the dopamine agonist bromocriptine would affect onset of anoestrus, voluntary food intake, body weight, and wool growth in a seasonal breed of sheep. Groups of eight Scottish Blackface ewes were injected i.m. each week with either the vehicle (Group A) or 2.0 mg (Group B), 6.0 mg (Group C), or 18.0 mg (Group D) of bromocriptine in a long-acting formulation, commencing on 18 January and terminating on 25 July (midwinter to midsummer in the northern hemisphere). Immediately before the bromocriptine injection, blood samples were taken for progesterone and prolactin determination. Voluntary food intakes were measured daily, and body weights were recorded every fortnight. Estimates of wool growth were made by weighing wool clipped from a measured area of skin once a month. Treatment had no effect on onset of anoestrus, voluntary food intake, body weight, or wool growth. Plasma prolactin concentrations increased significantly in all groups during the treatment period. From January to April, all doses of bromocriptine significantly reduced prolactin concentrations but later in the study (May and June) prolactin was significantly suppressed in Group D only, although even in this group prolactin concentrations increased between March and June. Pituitary prolactin content, measured at the end of the study in July, was also suppressed by bromocriptine. The gradual increase in prolactin concentrations in ewes receiving chronic bromocriptine was further investigated by treating a fifth group of ewes (Group E) with 18.0 mg of long-acting bromocriptine each week, commencing on 20 June.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Bromocriptine transcriptionally activates the multidrug resistance gene (pgp2/mdr1b) by a novel pathway.

The P-glycoprotein (Pgp) reversing agent, reserpine, induces MDR1 mRNA and PGP protein in human colon carcinoma cells (Schuetz, E. G., Beck, W. T., and Schuetz, J. D. (1996) Mol. Pharmacol. 49, 311-318) and in H35 rat hepatoma cells. Reserpine's interference with cellular dopamine utilization suggested that dopamine and dopaminergics might be important physiological regulators of PGP expression. Initial studies demonstrated that the H35 cells express the D2 dopamine receptor. Pgp protein and pgp2/mdr1b mRNA was increased (maximum of 10- and 8-fold, respectively) by the potent D2 dopamine receptor agonists bromocriptine, R(-)-propylnorapomorphine hydrochloride, and quinpirole, and Pgp protein induction was blocked by D2 receptor antagonists spiperone and clozapine. D2 receptor agonist induction of pgp2/mdr1b mRNA was paralleled by transcriptional activation of the pgp2/mdr1b promoter but blocked by pretreatment with the D2 dopamine receptor antagonists, spiperone, eticlopride, and clozapine. Co-transfection of a D2 dopamine receptor expression vector enhanced bromocriptine's transcriptional activation of the pgp2/mdr1b promoter. The G-protein, Galphai2, is required for bromocriptine transcriptional activation because the G-protein inhibitor, pertussis toxin, suppressed bromocriptine's activation of pgp2/mdr1b transcription and co-transfection of a dominant negative Galphai2 abrogated bromocriptine activation of pgp2/mdr1b. Gi proteins can transduce signals by activation of mitogen-activated protein kinases (MAPKs), and because Raf-1 is a known activator of MDR1, we tested for Raf-1 involvement. Co-transfection of a dominant negative Raf-1 failed to block bromocriptine induction of pgp2/mdr1b, and bromocriptine treatment caused no phosphorylation of the MAP kinase kinase substrates p42 and p44, demonstrating that the MAP kinase pathway was not involved. These are the first studies demonstrating transcriptional activation of an MDR gene by dopamine receptor agonists and that this activation occurs by a signal transduction pathway requiring the D2 dopamine receptor coupled to a functional G-protein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Bromocriptine treatment in a murine Parkinson's model: ultrastructural evaluation after dopaminergic deafferentation.

The objective of this article was to identify the effects of bromocriptine on the ultrastructure of the caudate nucleus in rats with a 6-hydroxidopamine (6-OHDA) unilateral lesion of the substantia nigra pars compacta. Eighteen Wistar male rats were stereotactically lesioned with 6-OHDA (n=12), or sham lesioned (n=6). Two days after rotational behavior was tested, and 2 days later, 6 rats were treated with 0.3 mg/Kg bromocriptine orally for a month and 6 rats were kept for the same time without treatment. The neuropile of the sham operated and bromocriptine-treated rats was well preserved contrary to the non-bromocriptine-treated rats. Also, it was found that there was a significant difference in the number of synaptic endings with edema in caudate of bromocriptine-treated rats compared with non-treated rats; however, the size of the synaptic endings were different to those found in the sham lesioned rats. Also, as in the sham lesioned group, the bromocriptines showed more synaptic contacts with dendritic spines contrasting to the non-treated group. The results suggest that bromocriptine possesses antioxidant properties because it decreased the ultrastructural alterations after 6-OHDA lesion.

Animals↗