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PubMed1981

Phenoxybenzamine and bromocriptine attenuate need for REM sleep in rats.

Phenoxybenzamine (10 mg/kg, IP), an alpha-adrenoreceptor blocker, and bromocriptine (5 mg/kg, IP), a dopamine receptor stimulant, were administered to rats while the animals were being deprived of REM sleep by selective REM sleep deprivation method. We have shown recently that alpha-adrenoreceptor blockers and bromocriptine when administered to rats after the animals had been deprived of REM sleep were able to abolish REM sleep rebound and thus attenuate the need for REM sleep. The purpose of this study was to investigate whether these agents might also have the capacity to attenuate the need for REM sleep when given to animals in a situation when the need for REM sleep is being generated, i.e. during REM sleep deprivation. Our results show that administration of phenoxybenzamine or bromocriptine to rats immediately before or during the period of REM sleep deprivation also abolished appearance of subsequent REM sleep rebound. This suggests that administration of the two pharmacological agents prevented the generation of REM sleep pressure by fulfilling the need for REM sleep.

Animals↗
PubMed1983

Bromocriptine promotes recovery of self-stimulation in 6-hydroxydopamine-lesioned rats.

Rats with stable self-stimulation response rate-current intensity functions were subjected to bilateral 6-hydroxydopamine injections into the substantia nigra. The effect of several drug treatments were evaluated on the 6-hydroxydopamine lesion self-stimulation deficit. d-Amphetamine (1.0, 2.0 and 3.0 mg/kg) and scopolamine (0.25, 0.5 and 1.0 mg/kg) had little or no effect on self-stimulation, but bromocriptine (2.0 and 4.0 mg/kg) produced a nearly complete recovery of self-stimulation performance. In contrast, scopolamine increased locomotor activity: whereas, bromocriptine did not increase activity. These results point up the efficacy of bromocriptine in reversing self-stimulation deficits induced by a dopamine deficiency, and indicate that self-stimulation may be a more useful behavior than locomotor activity for evaluating drugs which might alleviate Parkinsonism.

Animals↗
PubMed1994

Bromocriptine treatment increases lipolysis and steady-state levels of G proteins in adipocytes from lactating rats.

An increase in the rate of lipogenesis and a decrease in the lipolytic response to catecholamines can be observed in adipocytes after weaning or litter removal. Bromocriptine treatment of lactating rats also produces an increase in lipogenesis but fails to decrease the lipolytic response of adipocytes to catecholamines seen after weaning or litter removal. No changes in total number or affinity of beta-adrenergic receptors or adenosine A1 receptors were detected by bromocriptine treatment using radioligand binding assays. However, we observed an increase in the amount of radioactivity from [32P]NAD+ incorporated into alpha-Gs (192 +/- 26%) and alpha-Gi (178 +/- 33%) by cholera- and pertussis-toxin-catalyzed ADP-ribosylation, respectively, with the same treatment, Immunoblotting using RM/1 and AS/7 antisera, which specifically recognize alpha-Gs and alpha-Gi 1,2, respectively, confirmed the increase in the steady-state levels of these G-protein alpha-subunits. The increase in the steady-state levels of alpha-Gs may account, at least in part, for the increased lipolytic response of adipocytes to catecholamines in bromocriptine-treated rats.

Adenosine↗
PubMed1996

[Pleural effusion and severe edema of the lower limbs induced by bromocriptine].

High doses of bromocriptine used for treatment of Parkinson's disease may be associated with pleuropulmonary complications. Isolated pleural effusions are a rare manifestation as is lower limbs edema are an exceptionally one. We report the case of a 67-year-old man, treated since five years by a daily dose of 30 mg of bromocriptine for Parkinson's disease, who developed important leg's edema and a few months later an exsudative right pleural effusion. No etiologies were found. Bromocriptine was discontinued. The evolution was characterized by nearly complete resolution of pleural effusion and disparition of lower limbs edema.

Aged↗
PubMed1988

Tamoxifen plus bromocriptine versus tamoxifen plus placebo in advanced breast cancer: results of a double blind multicentre clinical trial.

We carried out a double blind multicentre clinical trial in which 171 patients with advanced breast cancer were randomized to receive tamoxifen (30 mg/day) + bromocriptine (5 mg/day) or tamoxifen + placebo. No difference was found in the overall response rates in the two groups (37.5% for placebo; 38% for bromocriptine) or in subgroups (breast tumours, lymph nodes, lung, bone, skin metastases). Tolerability was good in both groups. Within the limits of the statistical power of the test (80%), our results do not show any benefit when bromocriptine was added to tamoxifen.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1982

Failure of dopamine and bromocriptine to affect prolactin release and cell growth in the dopamine receptor-deficient 235-1 clone.

The 235-1 clone was recently derived from the 7315a transplantable pituitary tumor and continues to secrete rat prolactin. The cells have a prominent Golgi apparatus which can be stained immunocytochemically for prolactin, but there were no 600-900 nm granules which are characteristic of normal mammotrophs. In a perfused cell-column apparatus, prolactin release from the clone was unchanged by dopaminergic agonists, thyrotropin-releasing hormone and estradiol but stimulated by dibutyryl cyclic AMP. Cellular cyclic AMP content was also not changed by dopamine but was dramatically enhanced by prostaglandin E1, indicating that at least one hormone-adenylate cyclase coupling mechanism was functional. In radioligand binding studies using the dopamine antagonist [3H]spiperone, no evidence of a dopamine receptor was obtained. The [3H]spiperone binding present was not stereoselective, and exceedingly high concentrations of other ligands were required to displace the binding. In addition, the induction of a prolactin-secreting hard tumor in rats by subcutaneous inoculation of the 235-1 cells failed to induce measurable dopamine receptors associated with the tumor cells. In order to address the possibility that there were functional dopamine receptors on these cells, but that they could not be resolved with either the cell column and cyclic AMP studies or the radioreceptor assay, the clone cells were incubated with 0.1-100 nM bromocriptine for up to 8 days. Bromocriptine had no effect on the growth rate or prolactin secretion of the 235-1 clone but inhibited prolactin release from anterior pituitary cells by over 73% in control studies. We conclude that the 235-1 clone does not express dopamine receptors and that the presence of dopamine receptors is obligatory for the typical inhibitory effects of bromocriptine on prolactin release and pituitary cell growth.

Animals↗
PubMed1988

Effects of bromocriptine on prolactin cellular hypertrophy, proliferation and secretory activity in diethylstilbestrol-induced pituitary tumors.

Pituitary tumors induced by chronic diethylstilbestrol (DES) treatment in female F344 rats were treated subsequently with bromocriptine (BC). Effects of BC on separable subpopulations of lactotrophs were examined. Enzymatically dissociated cells from individual pituitaries were assessed regarding total number, relative lactotroph population, intracellular prolactin (PRL) content, PRL release in primary culture, and density alterations by separation in Ficoll-Hypaque or after sedimentation at unit gravity. In addition to the treatment and analysis of in situ tumors, the effects of BC treatment in vitro were assessed, using tumor cells which were first separated on Ficoll-Hypaque. Cell proliferation was assessed by cell cycle analysis, using DNA measurement by laser flow cytometry. BC treatment of tumors reversed the effects of DES on pituitary weight, PRL content and in vitro PRL release. Total cell recovery was not affected by BC, but cell separation showed that BC reduced the number of larger PRL-containing cells. Cell cycle analysis showed a decrease in numbers of cells in S and G2 cycle phases after BC in only one of four experiments. BC had an effect on proliferation in only the upper gradient fractions, containing the smallest cells. Culture of Ficoll-separated tumor cells revealed greater PRL release among lighter/smaller cells. BC treatment inhibited PRL release from both light and dense cells. The results establish that PRL cell hypertrophy, as well as hyperplasia, results from DES treatment. Bromocriptine treatment reverses this hypertrophy concomitant with inhibiting PRL synthesis and release. Reversal of proliferation in tumor cells is not a major effect of bromocriptine treatment.

Animals↗
PubMed1995

Inhibitory effects of bromocriptine on phospholipid peroxidation induced by dopa and iron.

Membrane lipid peroxidation has been suggested to participate in the nigral degeneration of Parkinson's disease. In the present study, we demonstrate that bromocriptine inhibits lipid peroxidation in phospholipid liposomes induced by dopa and iron complexes. Because this lipid peroxidation is not mediated by active oxygen species, antioxidant properties of bromocriptine do not seem to be derived from radical scavenging effects in our experimental conditions. Bromocriptine had no scavenging effect on superoxide produced by hypoxanthine-xanthine oxidase when determined by the chemiluminescence assay using MCLA, a Cypridina luciferin analog, as a probe.

Bromocriptine↗
PubMed2005

The effect of selective sst1, sst2, sst5 somatostatin receptors agonists, a somatostatin/dopamine (SST/DA) chimera and bromocriptine on the "clinically non-functioning" pituitary adenomas in vitro.

The aim of the work was to investigate the effects of somatostatin analogs acting selectively on sst1 (BIM-23926), sst2 (BIM-23120) and sst5 (BIM-23206) receptor subtypes on the viability of "clinically non-functioning" pituitary adenomas in vitro. The effects of native SST (SST-14), a SST/DA chimera (BIM-23A387) and a D(2)-dopamine receptor agonist bromocriptine (BC) were also examined. The study was performed on 10 surgically removed pituitary macroadenomas, diagnosed before surgery as "non-functioning". A part of each tumor was mechanically dispersed and digested with collagenase to isolate the tumoral cells. Another part of each tumor was fixed, embedded in paraffin and immunostained to reveal the pituitary hormones and SST receptor subtypes (sst1, sst2A, sst2B, sst3, sst4, sst5). The tumoral cell suspensions were incubated for 24 h with the substances mentioned above. The quantity of viable cells was estimated using the EZ4U system. The results were compared with the immunohistochemical evaluation of the hormonal profile of adenoma and the sst receptor subtype immunoreactivities present. The findings indicate that selective sst1, sst2 and sst5 receptors agonists, SST/DA chimera and D(2)-dopamine receptor agonist bromocriptine affect the viability of some, but not all, "clinically non-functioning" pituitary adenomas in vitro. The most effective was bromocriptine. The investigated somatostatin analogs including SST/DA chimera exerted roughly similar inhibitory effects. Further studies are needed to fully evaluate the potential usefulness of these compounds in the pharmacological treatment of "non-functioning" pituitary tumors.

Adenoma↗
PubMed2005

Mixed neuronal-glial tumor of the fourth ventricle and successful treatment of postoperative mutism with bromocriptine: case report.

BACKGROUND: Tumors composed of both neurocytic and astrocytic cells are uncommon and poorly understood. We describe the clinicopathologic features of a very rare rosette-forming glioneuronal tumor of the fourth ventricle and propose bromocriptine as a useful therapeutic agent for cerebellar mutism after posterior fossa surgery. CASE DESCRIPTION: A fourth ventricle tumor was incidentally discovered in an 18-year-old woman. Magnetic resonance imaging revealed ventriculomegaly and a solid tumor with low-intensity signals on T1-weighted images and high-intensity signals on T2-weighted images. There was slight gadolinium enhancement. The tumor was subtotally resected. Although its lower half was well circumscribed, its upper half manifested invasive growth. Histologically, 2 components were identified, synaptophysin-positive neurocytic cells forming perivascular pseudorosettes and glial fibrillary acidic protein-positive astrocytic cells with Rosenthal fibers. Overall, cellular atypia was minimal and the MIB-1 labeling index was low. On the basis of these histologic findings, the tumor bore striking similarity to the recently described rosette-forming glioneuronal tumors of the fourth ventricle. Postoperatively, the patient manifested cerebellar mutism. The administration of bromocriptine improved her neurological status dramatically. CONCLUSION: The natural history of rosette-forming glioneuronal tumors of the fourth ventricle is not yet fully understood. Therefore, careful and long-term follow-up monitoring of the tumor hosts is necessary. Bromocriptine therapy may promote recovery from mutism after posterior fossa surgery.

Adolescent↗
PubMed1990

Visual function improvement in patients with macroprolactinomas treated with bromocriptine.

We studied eight patients who had visual field defects secondary to prolactin-secreting macroadenomas and who had improved visual function with bromocriptine treatment without surgery or radiation. We recommend bromocriptine as a primary treatment for prolactin-secreting macroadenomas. If therapy is effective, continued regular neuro-ophthalmologic, endocrine, and imaging studies are necessary, because treatment with bromocriptine must be continued indefinitely.

Adult↗
PubMed1998

Antiparkinsonian potential of interaction of LEK-8829 with bromocriptine.

The ergoline derivative, LEK-8829 (9,10-didehydro-N-methyl-(2-propynyl)-6-methyl-8-aminomethylerg oline), has been proposed as a potential atypical antipsychotic drug with antagonistic actions at dopamine D2 and serotonin 5-HT2 and 5-HT1A receptors (Krisch et al., 1994, 1996). LEK-8829 also induces contralateral turning in rats with 6-hydroxydopamine-induced unilateral lesion of dopamine nigrostriatal neurons. Turning is blocked by SCH-23390 (R(+)-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzaze pine), a dopamine D1 receptor antagonist. It has been suggested that LEK-8829 could have beneficial effects in parkinsonian patients suffering from psychotic episodes induced as a side-effect of antiparkinsonian treatment with dopamine D2 receptor agonists. Therefore, we now investigated the interaction of LEK-8829 with the dopamine D2 receptor agonist bromocriptine (2-bromo-alpha-ergokryptine) in 6-hydroxydopamine-lesioned rats. Treatment with either LEK-8829 (3 mg kg(-1)) or bromocriptine (3 mg kg(-1)) induced a vigorous contralateral turning response. The cumulated number of turns induced by the treatment with both drugs combined was not significantly different from the cumulated number of turns induced by single-drug treatment. The pretreatment with SCH-23390 (1 mg kg(-1)) did not have a significant effect on the bromocriptine-induced turning but significantly decreased the turning observed after the combined LEK-8829/bromocriptine treatment. We conclude that in the 6-hydroxydopamine model, the turning behaviour mediated by the LEK-8829/bromocriptine combination may be the result of opposing activity of both drugs at dopamine D2 receptors with concomitant stimulation of dopamine D1 receptors by LEK-8829. Therefore, LEK-8829 may have a potential for the therapy of parkinsonism complicated by dopamine D2 receptor agonist drug-induced psychosis.

Animals↗
PubMed1978

Value of luteinizing hormone-releasing hormone testing in bromocriptine treatment of amenorrhea and hyperprolactinemia in patients with pituitary tumors.

The results of bromocriptine treatment in 13 patients with radiologically evident pituitary tumors are described. A menorrhea was present in all patients, hyperprolactinemia in 12 of the 13 patients, and acromegaly in 3 patients. Five patients have previously been treated surgically and by radiotherapy because of suprasellar extension of the adenoma. Plasma prolactin levels after one single dose of 2.5 mg of bromocriptine were found to have no predictive value as to the dosage needed for treatment, whereas the plasma gonadotropin response after the administration of luteinizing hormone-releasing hormone appeared to be predictive with respect to the return of ovulation during bromocriptine therapy.

Adenoma↗
PubMed1981

Induction of ovulation in patients with normoprolactinemic amenorrhea by combined therapy with bromocriptine and clomiphene.

Bromocriptine is known to be effective in the treatment of women with hyperprolactinemic anovulation or amenorrhea-galactorrhea. A new schedule of combined treatment with bromocriptine and clomiphene citrate was applied to 23 patients with normoprolactinemic amenorrhea who failed to respond to clomiphene alone. Ovulation was restored by treatment in 14 of these patients (60.9%), resulting in pregnancy in 3 women. Treatment resulted in immediate suppression of serum prolactin levels and a gradual increase in serum luteinizing hormone levels and estradiol levels followed by a luteinizing hormone surge. The present results indicate that bromocriptine/clomiphene combination therapy is effective in the treatment of amenorrheic patients with normoprolactinemia who do not respond to clomiphene alone, and suggest that bromocriptine restores the responsiveness of the hypothalamic-pituitary-ovarian system to clomiphene.

Adult↗
PubMed1989

Prolactin suppression by bromocriptine stimulates aromatization of testosterone to estradiol in women.

The effect of follicular phase bromocriptine therapy on the ovarian endocrine response to clomiphene citrate and gonadotropins was studied in 35 tubal infertility patients in a randomized placebo-controlled trial. During bromocriptine treatment, the serum prolactin (PRL) concentration significantly decreased, and consequently the serum estradiol (E2) concentration was significantly higher than in the controls on cycle day 9, and the ratio of testosterone (T) to E2 was decreased from cycle day 8 through day 10. The luteal phase progesterone concentration and the length of the luteal phase were not affected by bromocriptine therapy. The number and quality of oocytes harvested and the cleavage rates were similar in both groups. The present results, together with our previous observations, demonstrate that PRL participates in the regulation of ovarian steroidogenesis, particularly aromatization of T to E2.

Adult↗
PubMed1998

Hyperprolactinemic recurrent miscarriage and results of randomized bromocriptine treatment trials.

OBJECTIVE: To evaluate hyperprolactinemia in the pathogenesis of recurrent spontaneous abortion. DESIGN: Randomized trial. SETTING: Miscarriage clinic, Yokohama City University Hospital, Yokohama, Japan. PATIENT(S): From a group of 352 women with recurrent spontaneous abortion, we identified 64 patients with a prolactin disorder that was not associated with any other etiologic abnormalities, including ovarian or endocrinologic disturbances such as luteal phase dysfunction, polycystic ovaries, hypersecretion of LH, galactorrhea, or thyroid hormone disorders. INTERVENTION(S): Restoration of prolactin levels with bromocriptine. MAIN OUTCOME MEASURE(S): Successful pregnancy (live birth). RESULT(S): The percentage of successful pregnancies was higher in the bromocriptine-treated group than in the group that was not treated with bromocriptine (85.7% versus 52.4%, P < .05). Serum prolactin levels during early pregnancy (5-10 weeks of gestation) were significantly higher in patients who miscarried (31.8-55.3 ng/mL) than in patients whose pregnancies were successful (4.6-15.5 ng/mL, P < .01 or P < .05). CONCLUSION(S): Appropriate circulating levels of prolactin may play an important role in maintaining early pregnancy, especially in cases of hyperprolactinemic recurrent miscarriage.

Abortion, Habitual↗
PubMed1979

Determination of bromocriptine in plasma: comparison of gas chromatography, mass fragmentography and liquid chromatography.

Gas chromatographic, mass fragmentographic and liquid chromatographic techniques for the determinations of bromocriptine (2-bromo-alpha-ergocriptine; Parlodel) in human plasma are described. These methods were found to be suitable for determining concentrations of bromocriptine down to 0.5, 1.0 and 10.0 microgram/l, respectively. Accuracy, specificity and analytical capacity were satisfactory for all three methods. Gas chromatography was compared with liquid chromatography, and the two methods were demonstrated to give identical results in patients treated with bromocriptine for Parkinson's disease. Gas chromatography was also compared with mass fragmentography, and the results from these two assays were also in agreement.

Bromocriptine↗
PubMed2001

Haloperidol-stomach lesions attenuation by pentadecapeptide BPC 157, omeprazole, bromocriptine, but not atropine, lansoprazole, pantoprazole, ranitidine, cimetidine and misoprostol in mice.

The focus was on haloperidol (central dopamine antagonist)-stomach lesion, a longly described suitable counterpart of dopamine blocker cysteamine-duodenal lesion. In this, the contribution of blockade of central/peripheral dopamine receptors and prostaglandins synthesis, along with influence of antiulcer agents was evaluated in mice. Male NMRI Hannnover mice were sacrificed 24 h after haloperidol (25 mg/kg b.w. i.p., given alone or with saline (haloperidol+saline) (i) or in combination (ii,iii)). Supporting central dopamine predominance for haloperidol stomach lesion induction, co-administration of peripheral dopamine receptor antagonist domperidone (5 mg/kg i.p.) (haloperidol+ domperidone) (ii), or prostaglandin synthesis inhibitor indomethacin (10 mg/kg s.c.) (haloperidol+ indomethacin) (iii) did not aggravate this lesion. (i) In haloperidol+saline challenged mice the lesions were inhibited by co-administration (/kg i.p.) of a gastric pentadecapeptide BPC 157, GlyGluProProProGlyLysProAlaAspAspAlaGlyLeuVal, M.W. 1419 (10 microg, 10 ng, 10 pg, but not 1 pg, 100 fg, 10 fg), bromocriptine (10 mg), omeprazole (10 mg, 100 mg, but not 1 mg). Atropine (10, 100, 200 mg), pirenzepine (10, 100, 200 mg), misoprostol (10, 100, 200 microg), pantoprazole (1, 10, 100 mg), lansoprazole (0.1, 1, 10 mg), cimetidine (10, 100, 200 mg) and ranitidine (10, 100, 200 mg) were not effective. (ii) Dopamine peripheral blockade influence: in haloperidol+domperidone mice, previously effective bromocriptine, pentadecapeptide BPC 157 (10 microg) or omeprazole (10 mg) did not attenuate stomach lesions. (iii) Prostaglandins synthesis blockade effect: in haloperidol+indomethacin mice, previously effective agents, bromocriptine or omeprazole were not active, while BPC 157 effect was only lessened.

2-Pyridinylmethylsulfinylbenzimidazoles↗