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PubMed1986

Effects of lactation and season on plasma prolactin concentrations and response to bromocriptine during lactation in the Bennett's wallaby (Macropus rufogriseus rufogriseus).

Prolactin concentration was measured in plasma collected each week for 13 months from lactating and non-lactating Bennett's wallabies (Macropus rufogriseus rufogriseus). In non-lactating animals, prolactin concentrations decreased towards the end of the study but such changes did not appear to fit a seasonal pattern. Prolactin concentrations were low during early lactation and at a similar level to non-lactating animals, increased significantly during late pouch life (February-May), and then returned to non-lactating levels at a time coincident with permanent exit of the joey from the pouch. Temporary removal of joeys from their mothers in April was followed by a rapid decline in prolactin concentrations which remained low for 24 h until the joey was returned to its mother, whereupon prolactin concentrations increased significantly within 2 h. The effect of a single injection of bromocriptine (5 mg/kg) on lactation, embryonic diapause and plasma prolactin concentrations was examined at two stages of lactation. In November (lactational diapause), bromocriptine had no effect on prolactin concentrations but two out of four suckling joeys died on days 13 and 14 after treatment, and three out of four females gave birth on days 27, 27 and 28. Bromocriptine treatment in April (seasonal diapause) was followed by a significant reduction in prolactin concentrations and reduced growth rate of joeys belonging to treated females. New births were not observed. In view of the effect of bromocriptine on plasma prolactin concentrations in late lactation and the demonstration that domperidone (a dopamine antagonist) significantly increases plasma prolactin concentrations, it would seem that dopamine can act as a prolactin inhibitory hormone in this as in other mammalian species.

Animals↗
PubMed1999

Effects of chronic bromocriptine (CB-154) treatment on the plasma glucose and insulin secretion response to neurocytoglucopenia in rats.

Neurocytoglucopenia has been reported to increase both parasympathetic and sympathetic tone with a predominant effect on the latter, which accounts for the major effect of plasma hyperglycemia and the inhibition of insulin secretion. The aim of this study was to determine the effects of chronic treatment with bromocriptine (0.4 mg/100 g body wt per day), a potent sympatholytic D(2)-dopaminergic agonist, on hyperglycemia and insulin secretion in response to neurocytoglucopenia induced by 2-deoxy-d-glucose (2DG). After 2 weeks of bromocriptine treatment the animals, freely moving in their cages, were submitted to 2DG administration (50 mg/100 g body wt) via atrial catheter infusion. After 2DG infusion, the plasma prolactin of vehicle-treated (VEH) rats increased rapidly, reaching a peak at 10 min (34.3+/-7.6 ng/ml; P<0.01). In contrast, 2DG infusion failed to induce any significant change in the plasma prolactin levels of bromocriptine-treated (BR) rats. BR rats showed higher resting glucose levels than control rats (8.2+/-0.28 mM (BR) vs 6.0+/-0.18 mM (VEH); P<0.01). However, the hyperglycemic response of BR rats to 2DG injection was 30% lower than that of VEH rats (P<0.05). BR rats also showed a rapid rise in plasma insulin levels reaching a peak at 30 min after 2DG injection (243% higher than basal values; P<0.01). This increased rise in the insulin response to neurocytoglucopenia of BR rats was blocked by previous intravenous injection of atropine methyl nitrate (0.2 mg/100 g body wt). The present results suggest that chronic treatment with bromocriptine determines a strong increase in the parasympathetic tone response to neurocytoglucopenia, which is responsible for the higher stimulation of insulin secretion observed in BR rats. The data also provide further evidence that D(2)-dopaminergic agonist can block neurocytoglucopenia-induced prolactin release.

Animals↗
PubMed1988

Therapeutic applications of bromocriptine in endocrine and neurological diseases.

Bromocriptine, or 2-bromo-alpha-ergocryptine, is a semisynthetic ergot alkaloid. The basis of its therapeutic application in endocrine and neurological diseases is its action as a potent dopamine agonist. Its ability to inhibit prolactin secretion has led to its successful use in suppression of puerperal lactation and in the treatment of pathological hyperprolactinaemia causing galactorrhoea, infertility or hypogonadism. It has been shown to be safe in pregnancy. The ability of bromocriptine to reduce the size of large prolactin-secreting pituitary tumours has resulted in the recovery of pituitary function and correction of visual field defects. Bromocriptine is less effective in acromegaly but is useful as adjuvant therapy to radiotherapy and/or surgery which has been the standard mode of treatment. It has been shown to be efficacious either alone or in combination with levodopa in the treatment of Parkinson's disease. Therapy with low doses appears to be effective and is associated with a significantly reduced incidence of side effects. The successful use of bromocriptine has also been reported for the treatment of non-functioning pituitary tumours, premenstrual syndrome, cyclical mastalgia, luteal phase insufficiency and portal-systemic encephalopathy, although its role in the treatment of these latter disorders remains uncertain until more extensive and adequately controlled trials have been conducted.

Bromocriptine↗
PubMed1984

Controlled study of bromocriptine and placebo for induction of ovulation in normoprolactinemic secondary amenorrhea.

In order to evaluate the effect of bromocriptine in the treatment of secondary amenorrhea, a double-blind placebo-controlled study including 30 women with normo-prolactinemic normo-hypogonadotropic hypogonadism was carried out. The patients were given either 5 mg bromocriptine or placebo every day for 12 weeks and observed during the following 3 months. A biphasic basal body temperature curve and serum progesterone levels exceeding 25 nmol/l during the expected midluteal phase were considered an indication of ovulation. Restoration of ovulation was observed in 2 of 17 women given bromocriptine and 4 of 13 women given placebo. Bromocriptine was found to have no specific effect on the restoration of ovulation in women with secondary amenorrhea and normoprolactinemic normo-hypogonadotropic hypogonadism.

Adolescent↗
PubMed1990

Prevention of breast pain and milk secretion with bromocriptine after second-trimester abortion.

Within 24 hours after abortion, 62 patients with a mean gestational age of 19 weeks, who had either induced (n = 50) or spontaneous (n = 12) abortions were randomly allocated to three groups: Group 1, bromocriptine 2.5 mg twice daily for 2 weeks; Group 2, placebo tablets 1 tablet twice daily for 2 weeks; Group 3, no treatment. Fifty-two patients completed the study (bromocriptine n = 18, placebo n = 18 and no treatment n = 16). Placebo had no apparent influence on breast symptoms. In both the placebo group and the untreated group, breast pain and milk secretion peaked on days 3 to 7, and milk secretion often continued for 3 weeks. Only 3/34 (9%) of untreated and placebo treated patients were free of breast symptoms. Compared with placebo, bromocriptine caused a significant reduction in the objective assessment score of breast tenderness (p less than 0.05) and milk secretion (p less than 0.01), in serum prolactin (PRL) (p less than 0.001) and in the subjective assessment score of breast pain (p less than 0.01) and milk secretion (p less than 0.01). Alleviation of breast pain and prevention of milk secretion appears to be indicated after second-trimester abortion, and treatment with bromocriptine is efficacious.

Abortion, Induced↗
PubMed1991

Psychotic exacerbation attributed to low-dose bromocriptine treatment of galactorrhea and hyperprolactinemia.

Low-dose bromocriptine administered for antipsychotic drug-induced hyperprolactinemia and galactorrhea precipitated an acute psychotic state in a female patient. Discontinuation of the bromocriptine and increase in antipsychotic dosage resulted in complete remission. We advise caution in the use of bromocriptine especially in patients with a pre-existing psychiatric history and recommend monitoring for changes in mental status when bromocriptine is prescribed.

Acute Disease↗
PubMed1996

Nasal spray bromocriptine: effects on serum prolactin in puerperal women.

BACKGROUND: The objective of this study was to investigate the effectiveness of a single nasal spray administration of 0.8 mg bromocriptine in reducing PRL serum levels. METHODS: Eighteen physiologically hyperprolactemic women in the early days of puerperium were randomized to receive nasal bromocriptine or placebo; PRL serum levels were measured by RIA at 45, 30 and 15 minutes before the administration and after the following times: 15, 30, 45, 60, 120, 180, 240, 300, and 480 minutes. RESULTS: After the administration of bromocriptine serum levels of PRL decreased rapidly; the reduction was statistically significant after 45 minutes. Four hours after the administration mean serum levels of PRL resulted in the normal range (< 20 micrograms/l); at the eighth hour the PRL levels were still normal. No one patient complained of any local or systemic side-effects. CONCLUSION: Nasal route seems to be an effective and probably safe administration route for bromocriptine.

Aerosols↗
PubMed1980

Plasma ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone responses to bromocriptine in normal men.

The effects of an initial oral 2.5 mg dose of bromocriptine and of a similar dose after treatment with 2.5--5 mg daily for one week on plasma concentrations of ACTH, cortisol, LH, FSH, testosterone, and dihydrotestosterone were studied in normal men. In addition to its suppressive effects on plasma concentrations of prolactin and catecholamines which have been reported previously, a single dose of bromocriptine produced small increases in plasma ACTH and cortisol. Neither a single dose of bromocriptine nor treatment for one week altered plasma concentrations of LH and FSH. Plasma concentrations of testosterone and dihydrotestosterone were not altered by a single dose of bromocriptine, but small increases in both were noted in some subjects after treatment for one week.

Adrenocorticotropic Hormone↗
PubMed1982

Bromocriptine therapy in oligozoospermic infertile men.

A prospective, randomized double-blind study with crossover using bromocriptine and placebo was performed on a group of 17 infertile males with idiopathic oligozoospermia. Twelve patients completed the duration of this study of eight months by receiving 5 mg of bromocriptine per day for four months followed by four months of placebo or vice versa. Prior to treatment, the sperm count was 8.76 +/- 1.32 (10(6)/ml). The hormonal profile was performed prior to treatment and included estimation of prolactin, T3, T4, thyroid stimulating hormone (TSH), testosterone, follicle stimulating hormone (FSH), and plasma LH. Stimulation studies using LHRH and TRH were also performed. All hormonal estimations were within normal limits. Compared to placebo, bromocriptine had no significant effect on sperm analysis, or basic hormonal profile. The stimulation test with luteinizing hormone releasing hormone (LHRH) was unchanged except for the basic plasma testosterone, which increased. The prolactin decreased following the thyrotropin releasing hormone (TRH) stimulation. Two pregnancies were noted four to six weeks following the end of treatment. Bromocriptine did not seem to be more effective than placebo in the treatment of idiopathic oligozoospermia.

Adult↗
PubMed1988

Effect of bromocriptine on neurophysin secretion in pregnant women in labour.

In order to determine whether dopamine plays a role in the control of neuropituitary function in pregnant women during labour, blood levels of nicotine (NSN)- and estrogen (ESN)-stimulated neurophysins were measured in 119 women treated orally with placebo (n = 59, control group) or 5 mg bromocriptine, a potent dopaminergic receptor agonist (n = 60, experimental group). Serum samples were taken before drug ingestion (basal sample) and at delivery. The serum basal concentrations of NSN and ESN were similar in both groups of pregnant women in labour. At delivery, serum ESN levels were similar in all women regardless of the treatment, whereas NSN concentrations were significantly lower in the bromocriptine-treated women than in those who were given placebo. In additional experiments the effect of 5 mg bromocriptine on the serum concentrations of NSN and ESN was tested for 6 hours after drug ingestion in 10 healthy, non-pregnant women and in 8 women in the 3rd trimester of pregnancy. Bromocriptine did not modify the circulating levels of NSN and ESN in either of these 2 groups of women. Since NSN and ESN are thought to be associated with vasopressin and oxytocin, respectively, these results indicate that in non-pregnant women and in pregnant women during late pregnancy dopaminergic stimulation with a dopaminergic receptor agonist does not inhibit the release of either vasopressin or oxytocin during rest. In contrast, dopaminergic receptor stimulation appears to play an inhibitory role in the regulation of vasopressin, but not oxytocin secretion in pregnant women in labour.

Adult↗
PubMed1985

Reduction of blood flow in the adenohypophysis of rats by bromocriptine.

The possibility that bromocriptine has a selective effect on blood flow in the adenohypophysis was examined in rats. Twenty-four anesthetized male Wistar rats underwent measurement of blood flow using the hydrogen clearance method. Intravenous injection of 50 micrograms/kg bromocriptine reduced the blood flow in both the medial and lateral parts of the adenohypophysis to about 70% of the baseline value. Simultaneously measured cerebral cortical and white matter flows were unchanged. Similar results were obtained following administration of a higher dose (500 micrograms/kg) of bromocriptine. This phenomenon cannot be attributed to the decrease in blood pressure. The course of change in blood flow in the medial and lateral adenohypophysis did not follow that of the mean arterial blood pressure, and the alteration of blood pressure remained within the limits of autoregulation in the adenohypophysis. The results indicate that bromocriptine is capable of reducing blood flow selectively in the pituitary region. This mechanism may contribute to the clinical usefulness of this drug.

Animals↗
PubMed1990

Hormonal dependency of cerebral meningiomas. Part 2: In vitro effect of steroids, bromocriptine, and epidermal growth factor on growth of meningiomas.

Cell culture and biochemical techniques have been employed to examine the effects of steroids, bromocriptine, and epidermal growth factor (EGF) on the growth and proliferative potential of meningiomas. In cell culture, the growth of meningiomas was not altered by progestogens, antiprogestogens, or 17beta-estradiol. The progestogen, norethisterone, had no effect on the uptake by meningiomas cell cultures of 3H-thymidine. Furthermore, cytosolic deoxyribonucleic acid (DNA) polymerase activity of meningiomas did not correlate with the progesterone receptor status of the same tumors. In contrast, the androgen antagonists, cyproterone acetate and 11-alpha-hydroxyprogesterone, and the dopamine agonist, bromocriptine, all inhibited the in vitro growth of meningioma cells. The growth of meningioma cell cultures was stimulated by EGF, and there was a positive correlation between the EGF content and DNA polymerase activity in meningioma cytosols. These results demonstrate that female sex steroids do not influence growth of meningiomas in vitro, whereas antiandrogens and bromocriptine have an antiproliferative effect. Consequently, bromocriptine and antiandrogens may have a role in the medical treatment of meningiomas. In addition, these results suggest that EGF may be involved in the genesis and/or progression of meningiomas.

Bromocriptine↗
PubMed1984

Bromocriptine inhibits growth hormone release from rat pituitary cells in primary culture.

The action of the potent dopamine receptor agonist bromocriptine was studied in primary cultures of rat anterior pituitary cells. Bromocriptine inhibited both prolactin and growth hormone release in a concentration-dependent manner. This effect was blocked by the dopamine receptor antagonist spiperone when the agonist and antagonist were added coincidently. In contrast, spiperone was unable to affect the actions of bromocriptine if added 1 min after bromocriptine application or later. These results suggest that dopamine receptors exist not only on mammotrophs, but also on somatotrophs in vitro.

Animals↗
PubMed1978

Treatment of acromegaly with bromocriptine.

Twelve patients with acromegaly were treated with bromocriptine for periods from nine to 23 months. All showed some clinical improvement. There was no significant difference in plasma growth hormone levels before and after therapy with bromocriptine, but a significant fall in plasma prolactin levels was observed after the bromocriptine therapy was commenced. The release of other pituitary hormones was not affected by bromocriptine.

Acromegaly↗
PubMed1984

Drugs five years later. Bromocriptine.

Bromocriptine, a specific dopamine receptor agonist, has been used for the treatment of various hyperprolactinemic conditions and as adjunctive therapy for acromegaly (with or without concomitant hyperprolactinemia) and Parkinson's disease. Bromocriptine is extremely effective in suppressing prolactin secretion regardless of the cause, in restoring gonadal function and fertility, and in decreasing the size of prolactin-secreting pituitary tumors. Most patients with acromegaly have clinical improvement with this drug. When bromocriptine is added to a regimen of levodopa or carbidopa, patients with Parkinson's disease frequently have additional clinical improvement and, in most patients, the levodopa or carbidopa dose can be reduced. Withdrawal of bromocriptine therapy is associated in most patients with reversal of its beneficial effects--return of hyperprolactinemia, return of excess growth hormone secretion, and exacerbation of Parkinson's disease.

Acromegaly↗
PubMed1984

Bromocriptine treatment of prolactin-secreting pituitary adenomas may restore pituitary function.

Six men with prolactin-secreting pituitary macroadenomas and deficiencies of pituitary hormones other than gonadotrophins were treated with bromocriptine for 6 months. During treatment the serum prolactin concentration decreased markedly in all six patients, and in four adenoma size decreased and visual function improved. Two patients who were hypothyroid before bromocriptine treatment were euthyroid during the sixth month of treatment, and the one patient who was hypoadrenal before treatment was euadrenal during treatment. Two of the six men who had subnormal growth hormone secretion before treatment had normal growth hormone secretion during treatment. We conclude that pituitary hormonal functions may improve during bromocriptine treatment for prolactin-secreting pituitary macroadenomas. This improvement may result from decompression of other pituitary cells, because correction of hypothyroidism by bromocriptine was accompanied by conversion from an absent to a normal thyrotrophin response to thyrotrophin-releasing hormone.

Adenoma↗
PubMed1999

Ergoline derivative LEK-8829-induced turning behavior in rats with unilateral striatal ibotenic acid lesions: interaction with bromocriptine.

LEK-8829 [9,10-didehydro-N-methyl-(2-propynyl)-6-methyl-8- aminomethylergoline bimaleinate] is an antagonist of dopamine D2 receptors and serotonin (5-HT)2 and 5-HT1A receptors in intact animals and a D1 receptor agonist in dopamine-depleted animals. In the present study, we used rats with unilateral striatal lesions with ibotenic acid (IA) to investigate the dopamine receptor activities of LEK-8829 in a model with innervated dopamine receptors. The IA-lesioned rats circled ipsilaterally when challenged with apomorphine, the mixed agonist on D1/D2 receptors. LEK-8829 induced a dose-dependent contralateral turning that was blocked by D1 receptor antagonist SCH-23390. The treatment with D1 receptor agonist SKF-82958 induced ipsilateral turning, whereas the treatment with D2 receptor antagonist haloperidol induced contralateral posture. The combined treatment with SKF-82958 and haloperidol resulted in a weak contralateral turning, indicating the possible receptor mechanism of contralateral turning induced by LEK-8829. Bromocriptine induced a weak ipsilateral turning that was blocked by haloperidol. The ipsilateral turning induced by bromocriptine was significantly potentiated by the coadministration of a low dose but not by a high dose of LEK-8829. The potentiation of turning was blocked either by SCH-23390 or by haloperidol. The potentiation of ipsilateral turning suggests the costimulation of D2 and D1 receptors by bromocriptine and LEK-8829, respectively, whereas the lack of potentiation by the highest dose of LEK-8829 may be explained by the opposing activity of LEK-8829 and bromocriptine at D2 receptors. We propose that the D2 and 5HT2 receptor-blocking and D1 receptor-stimulating profile of LEK-8829 is promising for the treatment of negative symptoms of schizophrenia.

Animals↗
PubMed1999

Differential effects of talipexole and bromocriptine on serotonin release from rat intestinal tissues--an in vitro study of the emetic response of antiparkinsonian dopamine agonists.

In order to elucidate the role of emetic action, the effects of talipexole and bromocriptine, two antiparkinsonian dopamine receptor agonists, on serotonin (5-HT) release from enterochromaffin (EC) cells were studied by measuring 5-HT concentrations in the perfusate of the isolated rat ileum. Bromocriptine (10(-8)-10(-6) M), which exerts agonistic effects on D1 and D2 receptors, increased 5-HT release in a concentration-dependent manner. No significant increase in 5-HT release was seen after addition of talipexole, which selectively stimulates D2 receptors and blocks 5-HT3 receptors, even at 10(-6) M. The increase in 5-HT release caused by bromocriptine at 10(-6) M was inhibited by administration of 10(-6) M of D1 receptor antagonist SCH 23390, D2 receptor antagonist spiperone, 5-HT3 receptor antagonist granisetron or tetrodotoxin (TTX). These results showed the involvement of both dopaminergic and serotonergic mechanisms in the 5-HT release from EC cells following the administration of dopamine receptor agonists. Bromocriptine might induce 5-HT release by stimulating D1, D2 and 5-HT3 receptors and depolarizing neurons in the ileum. On the other hand, talipexole might weaken 5-HT release from EC cells elicited by D2 receptor stimulation with its 5-HT3 receptor blocking property. It is suggested that the emetic effect of dopamine receptor agonists involves the peripheral gastrointestinal tract as their site of action.

Administration, Oral↗