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PubMed1981

Effect of bromocriptine, somatostatin, and oestradiol-17 beta on hormone secretion and ultrastructure of human pituitary tumours in vitro.

The effect of bromocriptine and somatostatin on hormone secretion and the ultrastructure of human pituitary adenomas was studied in vitro. Prolactin secretion was inhibited by bromocriptine in 3 out of 10 prolactin-secreting tumours and in explants from 2 normal pituitaries. GH secretion was reduced by bromocriptine in 4 out of 6 GH-secreting adenomas but was not affected by the drug in the incubations of normal pituitaries. Somatostatin inhibited GH secretion in 2 out of 5 pituitary adenomas and the effect was comparable with that of bromocriptine. Incubation of prolactin-secreting adenomas with oestradiol for as long as 24 days produced no change in hormone secretion. Examination of tumour explants by electron microscopy showed that somatostatin and bromocriptine produced accumulation of secretion granules but no changes in the secretory organelles. Long term bromocriptine treatment of "nude" athymic mice bearing xenografts of human pituitary adenomas suppressed hormone secretion and produced some increase in secretion granules but there were no morphological changes in the secretory organelles or other vital structures of the adenoma cells.

Adenoma↗
PubMed1981

Pituitary apoplexy in acromegaly during bromocriptine therapy.

Two cases of pituitary apoplexy occurring in the course of long-term bromocriptine therapy for active acromegaly are described. Although bromocriptine was effective in lowering serum growth hormone levels and concomitant clinical improvement was achieved, both patients developed an acute episode suggesting pituitary apoplexy when the therapy was continued for 6 and 24 months, respectively. Surgery verified marked haemorrhage and necrosis of an eosinophilic pituitary adenoma in each case. Bromocriptine may have suppressed the growth of these pituitary adenomas resulting in necrosis of the tumour, followed by haemorrhage into the adenoma. Pituitary apoplexy has not been documented as a complication of bromocriptine therapy. This report points out a possible role of bromocriptine in the development of this catastrophe and that careful follow-up is required when long-term treatment with bromocriptine is attempted.

Acromegaly↗
PubMed1984

Changes in plasma GH levels and clinical activity during bromocriptine therapy in acromegaly. The value of predictive tests.

Twenty-seven patients with active acromegaly despite previous treatment by surgery and/or radiotherapy received bromocriptine in a dose of 10-20 mg daily for a period of 6-9 months. The results of chronic bromocriptine treatment were evaluated by measurement of plasma growth hormone (GH) levels during the day and by subjective and objective criteria of clinical activity. The results of chronic bromocriptine treatment were also compared with four biochemical criteria obtained before treatment e.g. basal plasma prolactin (Prl) levels and the plasma GH response to oral administration of 2.5 mg bromocriptine respectively iv administration of 200 micrograms TRH and 500 micrograms somatostatin. The main observations may be summarized as follows: 1) The mean pre-treatment GH levels during the day ranged from 6-207 mU/1. Hyperprolactinaemia was present in 6 patients. 2) During bromocriptine treatment mean plasma GH levels decreased to less than 50% in 11 patients (GH responders) whereas in 19 patients changes of mean plasma GH and of subjective criteria of clinical activity were concordant. 3) Glucose tolerance improved significantly (P less than 0.01) in 10 GH-responders and the urinary hydroxyproline/creatinine ratio decreased significantly (P less than 0.05) in 8 GH-responders. 4) Five out of 6 patients with hyperprolactinaemia belonged to the group of GH-responders. 5) A single dose of 2.5 mg bromocriptine induced a more than 50% decrease of plasma GH in 8 of 11 GH-responders and in 5 of 16 GH non-responders.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1985

Bromocriptine therapy as pre-operative adjunct of non-functional pituitary macroadenomas.

Although bromocriptine administration produces reduction in size of prolactinomas, its effect upon non-functional pituitary adenomas is still uncertain. Nine patients with macroadenomas, 2 of them with prolactinomas and 7 with non-functional tumours, received bromocriptine prior to transsphenoidal surgery. Size reduction of tumour mass was assessed by computerized tomography and by visual field examination before and following bromocriptine treatment. There were no signs of size diminution or pathological changes in the non-functional adenomas treated pharmacologically during 15 to 360 days. Both patients with prolactinomas had radiological evidence of size reduction and morphological changes on microscopic examination. These 2 patients had tumours with prolactin granules (immunocytochemistry) and adenoma cells showed reduced cytoplasmatic, nuclear and nucleolar areas. Neither vascular damage, cell necrosis, nor infarction was observed by electron microscopy. Patients with non-functional tumours as determined by immunocytochemistry and hormone production did not benefit from bromocriptine. The suggestion that bromocriptine can be used as primary treatment for non-functional pituitary tumours is not supported by the present study. Conversely, in cases of macroprolactinoma, bromocriptine is a useful pre-operative adjunct when surgery is planned and for those patients in whom a surgical cure is considered difficult owing to the tumour size.

Adenoma↗
PubMed1976

Study of the suppression of lactation and the influence on blood clotting with bromocriptine (CB 154) (Parlodel): a double blind comparison with diethylstilboestrol.

Inhibition of lactation was studied in 38 puerperal women in a double blind trial to assess the effect of bromocriptine in comparison with diethylstilboestrol (DS). Simultaneously the influence of both compounds on blood clotting was studied, along with a control group of 20 women not receiving any medication. Bromocriptine was given in a daily dose of 5 mg for 14 days and DS in a daily dose of 20 mg for 7 days followed by a placebo for a further 7 days. The first doses were not later than 8 hours after delivery. Both compounds showed an inhibitory effect on the onset of lactation and mammary congestion. This inhibitory effect on both parameters was significantly in favour of bromocriptine during the last days of the treatment due to rebound in the DS group. The bromocriptine doses used (5 mg daily for 2 weeks) caused no objective side effects and no subjective restraint. Treatment with bromocriptine caused no untoward effect on the blood clotting, while in the DS group a slower return to normal antithrombin III could be observed. Also in this group one case of thrombophlebitis occurred. Bromocriptine can be administered to puerperal women for the suppression of lactation.

Blood Coagulation↗
PubMed2000

Effects of long-term pretreatment with isoproterenol on bromocriptine-induced tachycardia in conscious rats.

It has been shown that bromocriptine-induced tachycardia, which persisted after adrenalectomy, is (i) mediated by central dopamine D2 receptor activation and (ii) reduced by 5-day isoproterenol pretreatment, supporting therefore the hypothesis that this effect is dependent on sympathetic outflow to the heart. This study was conducted to examine whether prolonged pretreatment with isoproterenol could abolish bromocriptine-induced tachycardia in conscious rats. Isoproterenol pretreatment for 15 days caused cardiac hypertrophy without affecting baseline blood pressure and heart rate. In control rats, intravenous bromocriptine (150 microg/kg) induced significant hypotension and tachycardia. Bromocriptine-induced hypotension was unaffected by isoproterenol pretreatment, while tachycardia was reversed to significant bradycardia, an effect that was partly reduced by i.v. domperidone (0.5 mg/kg). Neither cardiac vagal nor sympathetic tone was altered by isoproterenol pretreatment. In isolated perfused heart preparations from isoproterenol-pretreated rats, the isoproterenol-induced maximal increase in left ventricular systolic pressure was significantly reduced, compared with saline-pretreated rats (the EC50 of the isoproterenol-induced increase in left ventricular systolic pressure was enhanced approximately 22-fold). These results show that 15-day isoproterenol pretreatment not only abolished but reversed bromocriptine-induced tachycardia to bradycardia, an effect that is mainly related to further cardiac beta-adrenoceptor desensitization rather than to impairment of autonomic regulation of the heart. They suggest that, in normal conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at peripheral dopamine D2 receptors.

Adrenergic beta-Agonists↗
PubMed1992

An acute remission of Reiter's syndrome in male patients treated with bromocriptine.

We describe 4 male patients with Reiter's syndrome treated with bromocriptine. All 4 had infectious gastroenteritis and chronic Reiter's syndrome with arthritis and enthesopathy that persisted despite treatment in 3 with antiinflammatory drugs and 1 with sulfasalazine for long periods. In all patients treatment was cancelled 8 days before bromocriptine treatment. In 2 patients a dramatic improvement was observed 24 h after 2.5 mg/day of bromocriptine. Two patients improved after 4 days of bromocriptine treatment (5 mg/day). All 4 patients remained asymptomatic for at least 4 months of bromocriptine treatment. Bromocriptine may be useful for treating male patients with Reiter's syndrome.

Adult↗
PubMed1992

Effects of cocaine alone and in combination with bromocriptine in human cocaine abusers.

This study was conducted to determine whether the acute administration of bromocriptine, a dopamine agonist, modulates the acute pharmacologic effects of i.v. cocaine in humans. Eight current users of i.v. cocaine who were not seeking treatment for their cocaine abuse completed the study while they were inpatients on a research unit. Twelve drug conditions were tested in all subjects in randomized order under double-blind, double-dummy conditions and included cocaine (0, 12.5, 25 and 50 mg, i.v.) in combination with bromocriptine (0, 1.2 and 2.5 mg given orally 2 hr before the cocaine injection). Physiologic and subject- and observer-rated responses were measured. Cocaine alone significantly increased pupil diameter, heart rate and blood pressure, and ratings of drug effect, good effects, liking and rush. Bromocriptine alone significantly increased pupil diameter and heart rate, decreased blood pressure and had only minor effects on subjective measures. There were significant cocaine/bromocriptine interactions on diastolic and mean arterial blood pressure, with combinations producing significantly smaller increases compared to cocaine alone, and on heart rate, with combinations producing significantly larger increases compared to cocaine alone. The physiologic and subjective effects of cocaine were not modified by pretreatment with bromocriptine in any other way that might indicate either a therapeutic benefit or a safety concern. However, bromocriptine alone produced undesirable effects (fainting) that should be considered before administration to outpatient cocaine abusers. Any possible therapeutic benefits of acute administration of bromocriptine in cocaine abuse are not likely to be due directly to modulation of the acute effects of cocaine.

Adult↗
PubMed2005

Hyperprolactinemia presenting with encephalomalacia-associated seizure disorder and infertility: a novel application for bromocriptine therapy in reproductive endocrinology.

OBJECTIVES: To describe successful oral bromocriptine therapy for hyperprolactinemia accompanied by seizure disorder and encephalomalacia identified during infertility evaluation. MATERIALS & METHODS: A 32 year-old male with an unspecified seizure disorder was referred for infertility consultation. The initial seizure was at age 12, and was treated sequentially with phenytoin, phenobarbitol, and carbamazepine monotherapy which was maintained for six years and then discontinued. At age 26, a second seizure was experienced and 150mg lamotrigine b.i.d. was initiated. When the patient married it was discovered that erection was impossible; tadalafil was administered without success. At our center, total testosterone was low at 107ng/dl and semen analysis revealed oligoasthenozoospermia. Serum prolactin was 79.3ng/ml; visual field examination was normal. Brain MR showed no pituitary enlargement. However, encephalomalacia of the right occiptal lobe with porencephalic dilation of the occipital horn of the right lateral ventricle was present. RESULTS: The patient was initially placed on 2.5mg/d bromocriptine but after three months only a nominal reduction of serum prolactin was achieved. Serum prolactin normalized (25.4ng/ml) after bromocriptine was increased to 7.5mg/d. Repeat semen analysis showed overall sperm concentration of 85M/ml, 30% motility and 12% normal forms morphology (Kruger strict criteria). Total testosterone level was 191ng/dl after final bromocriptine dose was attained, which was well tolerated. DISCUSSION: Bromocriptine has an established role in the management of hyperprolactinemia, particularly in women. For males with elevated serum prolactin even when associated with focal encephalomalacia and seizure disorder, bromocriptine therapy can offer safe benefits including improved semen parameters and normal serum testosterone levels.

Adult↗
PubMed1990

[Comparison of the therapeutic results of bromocriptine treatment of prolactin microadenoma and macroadenoma].

26 infertile women with prolactinomas were treated by bromocriptine, 24 of them (92%) became pregnant. All of 11 cases with microadenoma restored fertility, 13 out of 15 patients with macroadenomas became fertile. The total is 32 pregnancies. 4 of 32 pregnancies developed spontaneous abortion or fetal death in uterus. In all the women with microadenomas and 11 cases with macroadenomas there were no symptom of enlargement of pituitary tumor, 2 patients with macroadenomas developed visual field defect or paralysis of left oculomotor nerves. 22 patients continued bromocriptine medication for 4.6 +/- 3.6 months and in 6 patients took bromocriptine until delivery. No congenital malformation were found, the development and intelligence were normal in their children. 4 women with microadenomas restored menses at postpartum without taking bromocriptine. The other patients still suffered amenorrhea and galactorrhea after delivery. 8 patients breast-feed their infants for 17.9 +/- 9.5 (7-33) months, no harmful effect on prolactinomas was found. Our data suggest: (1) The pregnancy rate in women with prolactinomas treated with bromocriptine was 92%. (2) Women with microprolactinomas who became pregnant appear to have a very low risk for developing complications and women with macroprolactinomas should be followed closely throughout pregnancy for pituitary tumors enlargement. (3) Bromocriptine therapy do not increase the risk of spontaneous abortion in women with prolactinoma and congenital anomalies of their offspring during pregnancy.

Adult↗
PubMed1990

Bromocriptine produces decreases in cocaine self-administration in the rat.

The effect of bromocriptine pretreatment was investigated in rats trained to self-administer intravenous cocaine on a fixed-ratio (FR) 5 schedule of reinforcement. Bromocriptine, a dopamine agonist, produced dose-dependent decreases in cocaine self-administration at doses of 4.0, 8.0, 16.0, and 32.0 mg/kg. In a separate group of rats trained on a DRL 20-second schedule of food reinforcement used to produce the same overall rate of responding for food as for cocaine on the FR 5 schedule, bromocriptine did not produce a significant effect on overall response rate, number of reinforced responses, or percent of responses that were reinforced. Given that bromocriptine produced a specific effect on cocaine-maintained responding, the present results suggest that bromocriptine is interacting with the neurochemical substrate mediating the reinforcing effects of cocaine. The potential effectiveness of bromocriptine as a pharmacotherapy for cocaine dependence is discussed.

Animals↗
PubMed1988

Vaginal bromocriptine: pharmacology and effect on serum prolactin in normal women.

Oral bromocriptine treatment of hyperprolactinemia is frequently associated with gastrointestinal side effects. To assess the efficacy and safety of an alternate route of treatment, we randomly administered 2.5, 5.0, and 7.5 mg of bromocriptine vaginally to five normal women at 1-week intervals. Plasma bromocriptine and prolactin (PRL) levels were measured hourly for 12 hours, then every 2 hours for 12 hours after each dose. At the end of each study, the vagina was flushed with saline for measurement of residual drug. For comparison of serum PRL levels, six additional women were given 2.5 mg bromocriptine orally. After administration of 2.5, 5.0, and 7.5 mg vaginally, plasma bromocriptine was initially detectable at 5.4 +/- 0.4, 4.4 +/- 0.7, and 3.5 +/- 0.6 hours, respectively. For the same vaginal doses, the mean (+/- SEM) peak plasma levels were 555 +/- 164 pg/mL at 12 +/- 0.6 hours, 702 +/- 252 pg/mL at 11.2 +/- 0.9 hours, and 1055 +/- 220 pg/mL at 10.7 +/- 1.7 hours, respectively. After each dose, there was a slow decline in plasma bromocriptine levels, remaining above 50% of peak values at 24 hours. Less than 1% of the administered drug was recovered from the vagina at 24 hours. The pattern of PRL inhibition with all three doses was similar. The mean plasma PRL level decreased by 7 hours, the maximum PRL decrease (64 +/- 3, 75 +/- 1, and 66 +/- 4% after 2.5, 5.0, and 7.5 mg, respectively) occurring at 11 hours, and the plasma PRL levels changed little during the remaining 13 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Intravaginal↗
PubMed1988

Bromocriptine in polycystic ovarian disease: a controlled clinical trial.

Bromocriptine and placebo were given to a group of 20 polycystic ovarian disease patients on a double-blind, cross-over basis. Patients were studied for three cycles: a baseline cycle without any medication, a placebo-treated cycle, and a bromocriptine-treated cycle with multiple plasma samples taken during the different phases of the menstrual cycle. The clinical response to bromocriptine was compared with that of a placebo for the following hormones: prolactin (PRL), luteinizing hormone (LH)/follicle-stimulating hormone (FSH) ratio, testosterone, androstenedione, estradiol-17 beta (E2), estrone (E1), and progesterone. Patients were divided into two subgroups: hyperprolactinemic (basal PRL greater than 20 ng/mL) and normoprolactinemic (basal PRL less than 20 ng/mL), and the response of both subgroups to bromocriptine was compared. Prolactin, LH/FSH ratio, testosterone, and E1 showed a significant drop with bromocriptine, whereas E2 significantly increased. Two out of nine amenorrheic polycystic ovarian disease patients menstruated during bromocriptine treatment, and three patients showed evidence of ovulation.

Adolescent↗
PubMed1988

Dopaminergic effects on kidney function and responsiveness of aldosterone, plasma renin activity, prolactin, catecholamines, and blood pressure to stimulation in patients with prolactinoma. Comparison of the efficacy of pergolide and bromocriptine therapy.

8 beta-[(Methylthio)methyl]-6-propylergoline (pergolide) is a new, potent, long-acting dopaminergic DA2 receptor agonist currently being investigated for therapeutic use in patients with hyperprolactinemia, acromegaly or Parkinsons's disease. Since the influence of bromocriptine, a well-established dopaminomimetic compound, on aldosterone responsiveness and plasma renin activity is still a matter of debate, the efficacies of both compounds on these parameters and on kidney function, blood pressure, catecholamine release and prolactin levels were compared in 16 patients with prolactinoma. Supine and furosemide (40 mg i.v.)-stimulated plasma renin activity and aldosterone levels were similarly decreased by bromocriptine (2.5-30 mg/d) and pergolide (50-500 micrograms/d). Suppression of blood pressure, inhibition of stimulated norepinephrine release, increase in creatinine clearance, and decrease in base-line prolactin levels were similarly pronounced during treatment with both compounds. Metoclopramide (10 mg i.v.)-induced stimulation of aldosterone and prolactin levels, however, were suppressed only by bromocriptine and not by pergolide. It remains to be studied whether this difference between bromocriptine and pergolide is due to a potential agonist effect of pergolide on dopaminergic DA1 receptors which are influenced by bromocriptine in an antagonistic manner, or whether pergolide can be more readily displaced from its receptors than bromocriptine.

Adult↗
PubMed1985

Bromocriptine: problems with low-dose de novo therapy in Parkinson's disease.

Twenty Parkinson's disease patients, who had not yet received levodopa, were treated with low-dose bromocriptine. At a mean daily bromocriptine dose of 13.2 mg, 13 patients (65%) improved and had a 32% reduction in the combined score for tremor rigidity and bradykinesia. Adverse effects were frequent, and 25% of the patients were taken off the drug because of nausea or vomiting. After 30 months follow-up, only three patients continued on bromocriptine alone. Ten patients were eventually maintained on low-dose bromocriptine and levodopa-carbidopa, and a clear synergistic effect of bromocriptine in this drug combination was documented in eight patients. Low-dose bromocriptine does not replace levodopa as initial therapy for Parkinson's disease. The potential long-term benefit of the early use of combined low-dose levodopa-dopamine agonist therapy needs to be further studied.

Adult↗
PubMedDate not supplied

Effects of bromocriptine on the heart and the peripheral circulation of anesthetized cats.

Dopaminergic stimulants such as bromocriptine have multiple effects on the circulation. Based on dose-response curves obtained in preliminary experiments, we compared the effects of 30 micrograms/kg bromocriptine and 0.4 mg/kg dihydralazine infused intravenously over a period of 10 min into seven chloralose-urethane-anesthetized cats each. A third group of cats received placebo solution. The effect of both drugs on blood pressure was comparable, but other systemic hemodynamic variables and regional blood flows, measured with tracer microspheres, were altered differently. Bromocriptine lowered heart rate, did not change cardiac output, and increased total peripheral conductance modestly, whereas dihydralazine produced marked increases in cardiac output and total peripheral conductance. Bromocriptine dilated the vascular beds of the brain, kidneys, adrenal glands, and skeletal muscle without increasing flow through most of them. Dihydralazine caused striking vasodilation in the heart, brain, small intestine, and colon and a modest increase in conductance in the kidneys, adrenal glands, and skeletal muscle. Flow through the heart, brain, small intestine, and colon was increased. Vasoconstriction was observed in the pancreas with bromocriptine and in the liver, spleen, and, to a small extent, pancreas with dihydralazine. The distribution of effects was somewhat similar to the effects of dihydropyridine-derived calcium antagonists. With dihydralazine the fall in blood pressure was caused by peripheral vasodilation only, whereas with bromocriptine both peripheral vasodilation and effects on the heart contributed to the fall in blood pressure.

Anesthesia, General↗
PubMed1983

Bromocriptine in severe adult asthma--a negative report.

A pilot study had suggested that bromocriptine (a dopamine agonist) might be of benefit in severe asthma, particularly in patients with marked diurnal variation in peak flow. Two studies are reported: (1) a longterm double-blind, controlled trial comparing bromocriptine (B) with placebo (P) in patients with severe asthma and, (2) a withdrawal study in patients who had received known bromocriptine, with apparent benefit, for at least one year. Of 27 patients (16B, 11P) admitted to the double-blind trial only eight (4B, 4P) completed 52 weeks on the trial drug as nine (6B, 3P) had been withdrawn for side-effects, eight (4B, 4P) for failure and two (2B) for both reasons. The results, based on changes in steroid dosage and other medication, daily symptom scores and PEF values, suggest that bromocriptine has little effect in asthma. In addition side-effects were frequent and troublesome. In the withdrawal study, ten patients who had been taking bromocriptine for a year or more were switched to an indistinguishable placebo if their asthma was considered to be stable. The results, of this second study, support the conclusion of the double-blind study, that bromocriptine has little beneficial effect in asthma.

Adult↗
PubMed1984

Effect of various neuroactive drugs on bromocriptine concentration in the striatum of rats.

Parkinsonian patients are usually given several drugs concomitantly with bromocriptine, with variable results. The possibility of interference of these drugs with the availability of bromocriptine in the brain was investigated by measuring bromocriptine concentrations in the striatum in rats. After a single injection, bromocriptine concentration in the striatum was 13.1 +/- 2.9 ng/mg protein. Naloxone, an opiate receptor blocker, was found to produce the largest increase in bromocriptine content (21.7 +/- 2.5 ng/mg protein). Amantadine, diazepam and haloperidol produced the largest decreases (3.2 +/- 0.9, 3.3 +/- 0.8 and 4.4 +/- 1.2 ng/mg protein, respectively). Rats given L-dopa or benzodiazepine also showed slightly lower levels of bromocriptine.

Animals↗