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PubMed1984

[Size reduction of a nonfunctioning pituitary adenoma after bromocriptine therapy: case report].

Bromocriptine therapy may cause regression of prolactinomas and GH producing adenomas, but there is only few reports about the effect of bromocriptine against nonfunctioning pituitary adenomas and there is no reports about its histopathological changes. We report a nonfunctioning pituitary adenoma, which remarkably regressed during and following bromocriptine therapy. A 47-year-old man developed blurred vision on January 20, 1981. He was pointed out of bitemporal hemianopsia and of his left palor optic fundus. His endocrinological condition was panhypopituitarism and no hypersecreting hormones were found. Cranial computerized axial tomography showed huge dumbbell shaped high density mass extending from the enlarged intrasellar area to the floor of the third ventricle. On treatment with bromocriptine, 5 mg daily for 3 days, his visual acuity and field was remarkably improved. Treatment was continued with gradually increased doses of bromocriptine to 15 mg and so, remarkable shrinkage of tumor size about 50% was seen by computerized axial tomography by a month. In addition, by eight months, the tumor reduced to 22%. Transsphenoidal surgery revealed centrally necrotic tumor mass surrounded by peripheral fibrous one. Because of fibrous and hemorrhagic tumour, we could not remove it totally. The pathological specimen was examined by light and transmission electron microscopy. The tumor was diffuse-type chromophobe adenoma partially intersected by hypertrophied fibrous interstitial materials. Some tumor cells were stained faintly eosinophilic. The cytoplasms were shrunken and the tumor cells were clumped. The immunostaining of tumor was negative to all anterior pituitary hormones. The intracytoplasmic organellae, for example, rough endoplasmic reticulum, Golgi apparatus, were scanty but prominant deformed mitochondria and small secretary granules (the size of about 90-150 nm) were found by transmission electron microscope. We think that the tumor cells had various responsiveness to this drug and the one extreme was destruction of the nucleus, the irreversible change, and the other extreme was some cytoplasmic reduction, the reversible change. The histopathological changes were almost the same as those of prolactinomas treated with bromocriptine. In conclusion, the mechanism of shrinkage of nonfunctioning pituitary adenomas treated with bromocriptine is unclear but it is worth while treating inoperable or recurrent large nonfunctioning pituitary adenomas with bromocriptine.

Adenoma↗
PubMed1981

[Effects of bromocriptine on FSH and LH secretion in women with euprolactinemic anovulation (author's transl)].

A few reports have been given that Bromocriptine effected not only on the hyperprolactinemic anovulations but also on the euprolactinemic anovulations. This study was performed to examine the underlying mechanism, 5 mg of Bromocriptine was daily administered for 30 days to 38 women with euprolactinemic anovulations. The basal secretions of FSH, LH and Prolactin and also the responsiveness to LH-RH, TRH and estradiol were examined. 31.6% of oligomenorrhea, anovulatory cycle and Ist. grade amenorrhea showed ovulatory cycles, however, no ovulations were observed in IInd. grade amenorrhea. The basal levels of FSH and LH significantly increased but the basal levels of Prolactin decreased by Bromocriptine. The responsiveness of FSH to LH-RH was markedly promoted but LH showed no significant change. Serum FSH was suppressed in estrogen loading test after Bromocriptine, which was poorly changed before. On the other hand, serum LH was markedly elevated by estradiol after Bromocriptine, which showed poor elevation before. These results conclude that: 1) Ovulation is induced by Bromocriptine administration in euprolactinemic anovulations. 2) Bromocriptine promotes the FSH and LH secretion from the pituitary and also promotes the reserve of FSH in the pituitary. 3) Bromocriptine promotes the sensitivity of the estrogen feedback in the hypothalamus.

Adolescent↗
PubMed1982

Bromocriptine and glucose tolerance in acromegalics.

Acromegaly is very often accompanied by impaired glucose tolerance or a manifest diabetes mellitus, with increased immunoreactive insulin (IRI) levels whose response during oral glucose tolerance tests (OGTT) is quite often exaggerated. When the dopaminergic drug bromocriptine is administered to acromegalics, their elevated growth hormone (GH) levels very often decrease, their impaired glucose tolerance (as manifested in OGTT) improves and their exaggerated IRI response becomes more normal. Eighteen patients were treated with bromocriptine. They were followed-up repeatedly during their treatment of varying duration for up to 6 years. These results indicate that raised GH levels are not the only factor that impairs glucose tolerance in acromegalics. During bromocriptine administration, impaired glucose tolerance improved and abnormal IRI levels (OGTT) became more normal even without any decrease in the high GH levels. In non-diabetic acromegalics, when bromocriptine was administered, there was not only an average decrease in the elevated GH values during OGTT, but a normalization of increased IRI values as well, without any major change in the corresponding blood glucose levels. During insulin tolerance tests (ITT), after i.v. insulin, the IRI levels after 30 and 60 min were markedly higher in acromegalics on bromocriptine than in the same patients before its administration, without any significant change in the corresponding blood glucose values. In 2 diabetic acromegalics, bromocriptine administration re-established their lost ability to increase IRI levels during OGTT. This was accompanied by a marked improvement in their glucose tolerance. It is probable that bromocriptine decreases glucagon levels in acromegalics, or at least in some of them. It is suggested that bromocriptine could protect the beta-cells of acromegalics from "exhaustion'.

Acromegaly↗
PubMed1995

The response of "de novo" Parkinson's disease patients to bromocriptine in a "low and slow" regimen is predictive for prognosis.

It is possible that Bromocriptine only determines a complete antiparkinson effect in a subset of P.D. patients that have a good dopaminergic reserve. Our study intent to demonstrate that a good short-term response to Bromocriptine used in a "low and slow" regimen is a marker of long term good prognosis. We studied a series of 36 sequential "de novo" P.D. patients treated with Bromocriptine in a "low and slow" regimen. The principal end-point was the introduction of Levodopa. "Good prognosis" was defined as no need of Levodopa until five years of follow-up. An improvement greater than 33% in the Columbia rating scale, at the 6th month of treatment, was the cut-off point to decide that a patient had a good short term response to Bromocriptine. Nine patients fulfilled the criteria for being good short term responders. Multiple regression analysis showed that this outcome could not be predicted by the clinical characteristics of the patients at admission. The sensitivity and the specificity of the short term response to Bromocriptine to predict a good prognosis were 70% and 90.5% respectively. We conclude that Bromocriptine in monotherapy is an efficient antiparkinson agent in 1/3 of "de novo" P.D. patients and good short term response to Bromocriptine is an acceptable marker for a good prognosis. Therefore it is possible that the response to Bromocriptine is a discriminator for a subset of P.D. patients in the early phases of the disease.

Adult↗
PubMed1999

Bromocriptine-induced apoptosis in pituitary adenoma cells: relationship to p53 and bcl-2 expression.

In an attempt to understand the roles of the tumour suppressor gene p53 and the proto-oncogene bcl-2 in cell death and survival in pituitary adenomas, we investigated the relationship of their expression to the apoptotic response of two pituitary adenoma cell lines (GH3 and AtT-20) to bromocriptine. An MTT (3-4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrasolium bromide) assay was performed after treatment with bromocriptine for various periods of time over a range of concentrations to determine the effect of this drug on cell growth. Bromocriptine inhibited growth of GH3 and AtT-20 cells in a dose dependent manner. DNA fragmentation was assessed in GH3 and AtT-20 cells exposed to 10 ug/ml bromocriptine- for 48 h and 72 h. The DNA of GH3 and AtT-20 cells showed nucleosomal fragmentation, indicative of apoptosis. When assayed 2 days after adding bromocriptine, approximately 60% of GH3 and 58% of AtT-20 cells treated with bromocriptine displayed typical apoptotic morphology, including condensed chromatin and fragmented nuclei. There was a time dependent increase in the proportion of all tumour cells undergoing apoptosis. Decreased expression of bcl-2 and accumulation of wild-type p53 were associated with bromocriptine induced apoptosis in pituitary adenoma cells. DNA analysis confirmed the results obtained by the protein study. Different expression of p53 and bcl-2 genes is consistent with the expression of these gene products. These findings show that bromocriptine activated wild-type p53 and suppressed bcl-2 favouring occurrence of apoptosis in pituitary adenoma cells. Copyright 1999 Harcourt Publishers Ltd.

Journal Article↗
PubMed1996

MK-801 (dizocilpine): synergist and conditioned stimulus in bromocriptine-induced psychomotor sensitization.

Intraperitoneal injections of the D2/D3 dopamine agonist bromocriptine (5.0 mg/kg, IP) induced locomotion that became progressively stronger on successive days of testing. The sensitized response developed twice as rapidly when the non-competitive NMDA antagonist MK-801 (0.25 mg/kg, IP) was given 30 min after bromocriptine (so that the peak effects of the two drugs overlapped). In a second group of animals, MK-801 was given 30 min prior to bromocriptine (the pretreatment regimen typical of studies where MK-801 is reported to block cocaine, amphetamine or morphine sensitization) and locomotion was monitored during the pretreatment period; in this case sensitization to the locomotor-stimulating effects of MK-801 alone (in the pretreatment period) as well as sensitization to the locomotor-stimulating effects of the drug combination (following the second injection) were observed. No sensitization to the effects of MK-801 alone (pretreatment) were seen in animals that received saline rather than bromocriptine as their second injection in this experiment. Thus MK-801 does not block but rather enhances bromocriptine sensitization; it appears to do so by a synergism with the locomotor effects of bromocriptine and by becoming a conditioned stimulus for the sensitized response. These findings confirm the earlier report that NMDA receptor activation is not critical to bromocriptine-induced sensitization, and they illustrate the importance of controls for conditioning and state-dependency phenomena in studies of drug interactions in psychomotor sensitization.

Animals↗
PubMed2001

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

BACKGROUND: Long term levodopa therapy in Parkinson's disease is associated with the development of motor complications including abnormal involuntary movements and a shortening response to each dose (wearing off phenomenon). It is thought that dopamine agonists can reduce the duration of immobile off periods and the need for levodopa therapy whilst maintaining or improving motor impairments and only minimally increasing dopaminergic adverse events. OBJECTIVES: To compare the efficacy and safety of adjuvant cabergoline therapy versus bromocriptine in patients with Parkinson's disease, already established on levodopa and suffering from motor complications. SEARCH STRATEGY: Electronic searches of MEDLINE, EMBASE and the Cochrane Controlled Trials Register. Handsearching of the neurology literature as part of the Cochrane Movement Disorders Group's strategy. Examination of the reference lists of identified studies and other reviews. Contact with Pharmacia Upjohn Limited. SELECTION CRITERIA: Randomised controlled trials of cabergoline versus bromocriptine in patients with a clinical diagnosis of idiopathic Parkinson's disease and long-term complications of levodopa therapy. DATA COLLECTION AND ANALYSIS: Data were abstracted independently by the authors and differences settled by discussion. The outcome measures used included Parkinson's disease rating scales, levodopa dosage, off time measurements and the frequency of withdrawals and adverse events. MAIN RESULTS: Cabergoline has been compared with bromocriptine in five randomised, double-blind, parallel group studies including 1071 patients. Only one of the phase II studies was medium term (36 weeks), the others all being short term (12 -15 weeks). The non-significant difference in off time reduction produced by cabergoline compared with bromocriptine was 0.29 hours/day in favour of the former (weighted mean difference; 95% CI -0.10, 0.68; p = 0.15). Dyskinesia reported as an adverse event was significantly increased with cabergoline compared with bromocriptine (Peto odds ratio 1.57; 95% CI 1.05, 2.35; p = 0.03). Motor impairment and disability were measured in four of the studies using the UPDRS rating scale but the small differences in UPDRS ADL (part II) and motor (part III) scores were not statistically significant in any study. Similarly, no significant difference in Schwab and England score was seen. The number of patients rated as much or very much improved on a clinician's global impression scale was similar with both agonists. Levodopa dose reduction was no different between cabergoline and bromocriptine. There was more confusion with cabergoline (Peto odds ratio 2.02; 95% CI 1.09, 3.76; p = 0.03). Otherwise, dopaminergic adverse events were comparable with these agonists and no significant difference in all cause withdrawal rate was found. REVIEWER'S CONCLUSIONS: Cabergoline produces similar benefits to bromocriptine in off time reduction, motor impairment and disability ratings, and levodopa dose reduction over the first three months of therapy. Dyskinesia and confusion were increased with cabergoline but otherwise the frequency of adverse events and withdrawals from treatment were similar with the two agonists.

Antiparkinson Agents↗
PubMed1998

Ropinirole versus bromocriptine in the treatment of early Parkinson's disease: a 6-month interim report of a 3-year study. 053 Study Group.

We compared the efficacy and safety of ropinirole with that of bromocriptine after 6 months of treatment in a planned interim analysis of a 3-year, double-blind, randomized, multicenter study of 335 patients with early Parkinson's disease requiring dopaminergic therapy. Patients, treated with or without selegiline, received either ropinirole or bromocriptine. The mean Unified Parkinson's Disease Rating Scale (UPDRS) total motor examination scores (Part III) at baseline were similar in the four strata. Overall, and in the non-selegiline subgroup, the percentage improvement in the UPDRS total motor examination score was significantly higher for ropinirole than for bromocriptine, as was the proportion of "responders." In the selegiline subgroup, however, there was no significant difference between treatments. Similarly, in the non-selegiline subgroup, there was a significantly higher proportion of "improvers" on the Clinical Global Impression scale with ropinirole than with bromocriptine, whereas in the selegiline subgroup, there was no significant difference. Emergent adverse events occurred in 80% of patients in both treatment groups, the principal symptom in each group being nausea. The incidence of serious adverse events was low (3% for ropinirole, 6.6% for bromocriptine). The data indicate that (a) in the absence of selegiline, ropinirole is effective and superior to bromocriptine; and (b) selegiline does not affect the response in patients treated with ropinirole, but enhances the effects of bromocriptine.

Adult↗
PubMed1988

The motor effects of bromocriptine--a review.

For many years, bromocriptine has proven to be a useful treatment for some of the disabling motor effects seen in Parkinson's disease. As such, it has been the only commonly used directly acting D2 agonist available. But its mechanism of action has been obscure because many animal models indicated an absolute requirement for the presence of endogenous DA for bromocriptine to have any efficacy, despite its undoubted occupation of the D2 receptor with high affinity. Several scattered reports indicated, however, that bromocriptine could potentiate the effects of a number of other dopamine agonists (such as apomorphine and L-dopa) in a variety of pharmacological models and in the clinic. With the availability of SKF38393 and SCH23390, it soon became clear that bromocriptine, while a selective D2 agonist, depended in an absolute sense on the integrity of the D1 receptors. Thus, if SKF38393 was administered together with bromocriptine to rodents depleted of dopamine, marked locomotor excitation was produced, despite either drug alone being inactive. The present review explores the literature on the motor effects of bromocriptine and endeavours to integrate its behavioural, biochemical and electrophysiological effects into a coherent whole. It closes with a consideration of several remaining unsolved problems associated with the pharmacology of bromocriptine and suggests some future studies.

Animals↗
PubMed1993

Bromocriptine treatment over 12 years in acromegaly: effect on glucose tolerance and insulin secretion.

It is not known whether the beneficial effect of bromocriptine on glucose homeostasis in acromegaly is limited by a certain duration of therapy. To elucidate this problem, oral glucose tolerance tests were performed in 12 acromegaly patients before bromocriptine medication, under therapy (15.0 +/- 6.8 mg/day for 12 +/- 3 years), and during a 2-week drug withdrawal after long-term treatment. Initially altered glucose tolerance was normalized in 4 of 5 patients under bromocriptine therapy. During drug withdrawal the mean fasting glucose level and the mean glucose concentration at 120 min after oral glucose load increased from 5.05 +/- 0.61 to 5.77 +/- 0.78 mmol/l and from 5.61 +/- 2.05 to 7.55 +/- 3.05 mmol/l, respectively. A deterioration in glucose homeostasis was observed in 9 patients, and impaired glucose tolerance was ameliorated (but not to normal range) in 2 when bromocriptine was withdrawn. The proportion of alterations in glucose tolerance during drug withdrawal corresponded to that before the beginning of long-term bromocriptine treatment. Impaired glucose tolerance, observed in 2 patients under bromocriptine treatment, seemed to be compensated because a distinct elevation of glycosylated hemoglobin A1c was not observed. Bromocriptine led to a significant decrease in basal as well as glucose-stimulated insulin levels, and growth hormone secretion during oral glucose load was reduced in all 12 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1978

Subsensitivity of the rat striatal dopaminergic system after treatment with bromocriptine: effects on [3H]spiperone binding and dopamine-stimulated cyclic AMP formation.

Repeated daily administration of the dopamine (DA) agonist bromocriptine (15 mg/kg; s.cut.) to rats led to a time dependent decrease in the in vitro binding of [3H]spiperone to striatal membranes. Kinetic analysis of [3H]spiperone binding after 2 and 7 days of bromocriptine treatment showed a 25-50% reduction in the total number of binding sites with no changein their affinity for spiperone. There was also a decreased accumulation of cyclic AMP (cAMP) in striatal slices in response to DA after bromocriptine treatment. The DA-sensitive adenylate cyclase in striatal homogenates, however, remained unchanged in bromocriptine treated rats. There was also no change in cyclic nucleotide phosphodiesterase activity in striatal tissue after bromocriptine treatment. Furthermore, incubation of striatal slices in the presence of the phosphodiesterase inhibitor isobutylmethylxanthine did not alter the decreased cAMP response to DA after 2 days of bromocriptine treatment. These results suggest that a decreased number of DA receptor sites may be responsible for the reduced cAMP response to DA in striatal slices after bromocriptine treatment.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

The interactions of bromocriptine and lergotrile with dopamine and alpha-adrenergic receptors.

Bromocriptine and lergotrile, which are clinically used as antiparkinsonian (AP) agents, compete for the binding of H3-dopamine, H3-apomorphine, and H3-haloperidol to striatal membrane sites. Lergotrile has a higher affinity for the H3-dopamine binding to bovine striatal membranes than bromocriptine. Lergotrile and bromocriptine are almost equipotent in competing for the binding of H3-apomorphine to rat striatal membranes, but bromocriptine is more potent in competing for the binding of H3-haloperidol than lergotrile. These results indicate that lergotrile and bromocriptine are mixed putative agonist-antagonist with respect to the postsynaptic dopamine receptors. Lergotrile and bromocriptine at higher concentrations inhibit synaptosomal tyrosine hydroxylase activity, and reverse the apomorphine elicited enzyme inhibition. Thus, these ergot alkaloids behave as mixed agonist-antagonist also with respect to the presynaptic dopamine receptors. Bromocriptine and lergotrile, as well as other tested DH-ergot alkaloids and neuroleptics, compete for the binding of the alpha-antagonist H3-WB-4101 to rat cerebral cortical membranes. The displacing potencies of the tested DH-ergot alkaloids and of the neuroleptics indicate that they have a high affinity for the alpha-adrenoreceptors in the CNS.

Acetonitriles↗
PubMed1990

Effects of bromocriptine and desipramine on behavior maintained by cocaine or food presentation in rhesus monkeys.

This experiment tested whether bromocriptine or desmethylimipramine (DMI), both agents used clinically to treat cocaine abuse, could specifically alter behavior maintained by cocaine injections. Rhesus monkeys were trained to press a lever in daily experimental sessions under a three-component multiple schedule of reinforcement. In the first and third components, food was available under a fixed-ratio (FR) 30 schedule. In the second component cocaine (0.025 or 0.050 mg/kg/injection, IV) was available under a FR 30 schedule. Monkeys received continuous (24 h/day) IV infusions of several doses of bromocriptine or DMI. Bromocriptine (0.8-6.4 mg/kg/day) was infused for at least the same number of sessions as was required for responding to decline to low levels when the monkeys were allowed to self-administer saline. DMI (0.8-12.8 mg/kg/day) was infused for a minimum of 3 weeks. In some instances, low doses of bromocriptine decreased responding maintained by cocaine without reducing food-maintained responding, while higher doses of bromocriptine decreased responding maintained by either food or cocaine. However, bromocriptine doses that reduced cocaine intake also caused overt stimulation of locomotor activity. In contrast, DMI, at doses as much as 10 times higher than those used clinically to treat cocaine abuse did not affect responding maintained by cocaine or food. These results indicate that bromocriptine can selectively reduce behavior maintained by cocaine, although apparently by a mechanism other than blockade of reinforcing effects. On the other hand, DMI did not alter the reinforcing effects of either cocaine or food under these conditions.

Animals↗
PubMed1991

Evaluation of a repeatable depot-bromocriptine preparation(Parlodel LAR) for the treatment of acromegaly.

The effectiveness and side effects of a newly developed, repeatable depot-bromocriptine preparation, (Parlodel LAR, depot-bromocriptine), were studied in 7 acromegalic patients. A dose of 100 mg was injected at intervals of 28 days for 4 months, followed by 200 mg for 2 months. GH profiles (14 h) and an oral glucose load (oGTT) were performed prior to each injection. Depot-bromocriptine suppressed the mean serum profile GH concentration to less than 50% of the pretreatment value in 3 out of 7 patients (responders). Normalization of GH secretion was not achieved. During oGTT the mean serum GH concentration declined to 73%, 19% and 56% of the pretreatment value in the three responders (while on depot-bromocriptine 200 mg). IGF-I was reduced to 84% and 65% with 200 mg depot-bromocriptine in 2 GH responders only. No tumour shrinkage was observed in 3 patients with a visible tumor mass in NMR tomography. Side effects consisted of pronounced orthostatic dysregulation, nausea and vomiting on the day of injection in 3/7 patients. These results are comparable to the reported effectiveness and side effects of oral bromocriptine therapy. Depot-bromocriptine may be useful in selected responsive patients, particularly when compliance during oral therapy is a problem.

Acromegaly↗
PubMed1987

Influence of bromocriptine on free amino acids in the kidneys and heart of the rat.

The effects of bromocriptine, sulpiride or their combination on free amino acids in the kidneys and the heart after acute and chronic treatment of rats were investigated, using an automatic LKB Amino Acid Analyzer. Bromocriptine at a single dose of 4 or 10 mg/kg (i.p.) did not affect the level of any amino acid; however, at a dose of 20 mg/kg it significantly elevated the content of taurine in the kidney from 7.00 +/- 0.30 to 9.70 +/- 0.1 and in the heart from 22.9 +/- 1.7 to 30 +/- 1.2 mumol/g wet tissue (P less than 0.05, N = 7). It also increased glutamic acid in the heart from 3 +/- 0.1 to 4.5 +/- 0.25 mumol/g wet tissue (P less than 0.05, N = 7). Chronic oral treatment of rats with bromocriptine (20 mg.kg-1.day-1) for 5 weeks significantly elevated the level of taurine in the kidney from 7.2 +/- 0.3 (control) to 11.1 +/- 0.90 and in the heart from 23.1 +/- 1.7 to 38.8 +/- 1.8 mumol/l g wet tissue. It also increased cardiac glutamic acid content from 3 +/- 0.1 to 4.8 +/- 0.24 mumol/g wet tissue (P less than 0.01, N = 7). Concurrent administration of sulpiride (20 mg/kg) significantly suppressed bromocriptine-induced increases in taurine and glutamic acid in both organs, suggesting an activation of D2 receptors by bromocriptine. Due to the similarities between bromocriptine and the affected amino acids in renal and cardiac actions, it is suggested that mobilization of taurine and glutamic acid may at least in part contribute towards bromocriptine-induced renal and cardiac actions.

Amino Acids↗
PubMed1986

Bromocriptine inhibits incorporation of [3H]thymidine into rat pituitary tumor cells.

The effects of bromocriptine on GH3 pituitary tumor cell [3H]thymidine incorporation were studied. Cells were grown in the presence of bromocriptine, then exposed to a short-term pulse of [3H]thymidine in serum-free medium containing deoxycytidine (10 microM) to prevent deoxythymidine triphosphate (dTTP) pooling. After 48 h exposure to bromocriptine, basal prolactin (PRL)-secretion during 45 min was inhibited by 50% by 10 microM bromocriptine and thyroid releasing hormone-induced PRL stimulation was suppressed. Incorporation of radiolabelled thymidine into acid-precipitable DNA increased progressively from 15 to 60 min and was abolished by simultaneous incubation with excess unlabelled thymidine (100 microM). Bromocriptine (10 microM) inhibited incorporation of 5-50 microM [3H]thymidine, but this was not reversed by simultaneous incubation with metoclopramide (10 microM). Aminopterin, an inhibitor of endogenous de novo DNA synthesis, stimulated [3H]thymidine incorporation twofold and this increased DNA salvage pathway activity was also blocked by bromocriptine. As incorporation of [3H]thymidine into acid-soluble cell nucleotides was also inhibited by bromocriptine, the data suggest that in these cells the drug inhibits thymidine kinase activity, a salvage pathway of DNA synthesis.

Animals↗
PubMed1981

Bromocriptine compared to long-acting estrogens in lactation prevention: clinical efficacy, prolactin secretion and coagulation parameters.

Sixty-eight mothers who did not want to breast-feed their babies were submitted to one of the following regimes: an intramuscular injection of estrogen (25 mg) within 1 h after delivery (n = 24) or the administration of bromocriptine for 15 or 23 days (n = 21 and 23, respectively). A careful clinical evaluation was performed every day by the same examiner during the first 7 days postpartum; blood samples were collected on days 0, 3 and 5 for human prolactin (hPRL) and estradiol, also in some cases on day 17; assays were measured by radioimmunoassay. An evaluation of the coagulation parameters was performed on day 5 in 9 estrogen-treated patients and in 25 bromocriptine-treated patients. Only 5 (11%) out of the 44 patients treated with bromocriptine experienced at least one undesirable effect of breast engorgement, in contrast to 16 (67%) out of the 24 estrogen-treated patients; this difference was statistically highly significant (P less than 0.001). Dizziness was a significant side-effect of bromocriptine treatment, occurring in 20% of the cases. In the patients in whom the administration of bromocriptine was withdrawn after 15 days, a significant mean rebound elevation of hPRL levels above the normal range occurred on the 17th day. The latter observation gives some support to earlier proposals to continue bromocriptine for up to a total 3 wk in order to avoid rebound lactation. There was no significant alteration of fibrinogen, Howell time, activated partial thromblastin time (APTT), prothrombin time (PT), thrombin time and coagulation time; mean plasminogen levels were comparable in both treated groups, while mean antithrombin III levels were increased in the bromocriptine-treated group. The significance of the latter finding requires further evaluation.

Antithrombin III↗
PubMed1986

Bromocriptine enhances the behavioural effects of apomorphine and dopamine after systemic or intracerebral injection in rats.

The ergot alkaloid bromocriptine, given intraperitoneally produced dose-dependent, long-lasting stereotyped behaviour in rats which was partly antagonised by the injection of trifluoperazine into the caudate nucleus. The stereotyped behaviour produced by apomorphine (s.c.) in both naïve and catecholamine-depleted rats was significantly enhanced by prior treatment with bromocriptine (i.p.). The bilateral application of bromocriptine (2.5-40 micrograms/side in either 0.5% tartaric acid or 50% propylene glycol aqueous vehicles) to the nucleus accumbens (NAC) of rats had no effect on locomotion over a 12 hr period after injection. In contrast, another ergot alkaloid, ergometrine, dissolved in the propylene glycol vehicle, and dopamine (DA) dissolved in either of the vehicles or in saline, produced marked stimulation of locomotion. As well as being inactive after direct application to the nucleus accumbens, bromocriptine (10-160 micrograms/side) did not induce stereotyped behaviour after bilateral injection into the caudate nucleus. However, the local application of bromocriptine (10 micrograms/side) to the nucleus accumbens, while itself inactive, significantly enhanced the locomotor stimulant effect of DA (5 micrograms/side) applied to the same nucleus. The data suggest that bromocriptine is able to enhance the effects of agonists such as DA and apomorphine at DA receptors, even under conditions where bromocriptine itself is inactive.

Animals↗