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PubMedDate not supplied

The effect of food and metoclopramide on the pharmacokinetics and side effects of bromocriptine.

The effect of food and metoclopramide on the pharmacokinetics of bromocriptine was investigated in 7 healthy subjects. Plasma concentrations of bromocriptine were measured by radioimmunoassay after a single oral dose of 7.5 mg bromocriptine. Maximal plasma concentrations of bromocriptine were slightly lower when the drug was given after breakfast. Bioavailability of the drug was not significantly reduced by food nor by metoclopramide pre-treatment. Side effects of bromocriptine were considerably reduced by metoclopramide pre-treatment (0.5 mg/kg); the decrease was about 83% as estimated from Table II.

Administration, Oral↗
PubMed2006

Long-term quiescence of ectopic Cushing's syndrome caused by pulmonary neuroendocrine tumor (typical carcinoid) and tumorlets: spontaneous remission or therapeutic effect of bromocriptine?

In 1990, a 55-yr-old woman was admitted to the Medical Department of our hospital for severe hypercortisolism complicated by secondary diabetes mellitus and serious hypokalemia. Although inferior petrosal sinus sampling did not show any significant difference between central and peripheral ACTH concentration, suggesting an ectopic source of ACTH secretion, diagnostic imaging was negative and Cushing's disease due to hyperplasia of the pituitary intermediate lobe was suspected. Medical treatment with bromocriptine and cyproheptadine led to a rapid and stabile normalization of adrenal function, so that after two months cyproheptadine was stopped and bromocriptine was tapered to a smaller dose. An attempt to discontinue medical treatment, carried out 3 yr later, was followed by a quick increase of ACTH and cortisol levels, which were normalized by the resumption of the bromocriptine. Adrenal function remained normal until 1994 when hypercortisolism relapsed despite the treatment. Chest radiography and computed tomography (CT) scan detected a 6 mm nodule in the middle lobe of the lung which proved to be a neuroendocrine tumor, with immunohistochemical positivity for ACTH. Nests of neuroendocrine cells (tumorlets) were also demonstrated in the surrounding lung tissue. After the lobectomy, the patient recovered completely from Cushing's syndrome and no symptoms and/or signs of recurrence have been observed over the subsequent follow-up period. Although cyclical spontaneous Cushing's syndrome could not be excluded, there was strong evidence that medical treatment with bromocriptine might have played a key role in long-lasting remission. To our knowledge, this is the second case described in literature of Cushing's syndrome caused by neuroendocrine lung tumor responsive to bromocriptine.

ACTH Syndrome, Ectopic↗
PubMed1987

Effects of a new long-acting form of bromocriptine on tumorous hyperprolactinemia.

Recently, a new long-acting form of bromocriptine (Parlodel LA, Sandoz) has been developed and it has already been found to be effective in lowering plasma PRL levels in normal volunteers and postpartum women. This work reports the clinical, hormonal and radiological effects of a single 50 mg dose of long-acting bromocriptine in 10 patients with tumorous hyperprolactinemia (2 microprolactinomas, 6 macroprolactinomas, 1 acromegaly and 1 nonsecreting macroadenoma). A rapid and long-lasting (28 days) normalization of PRL levels was observed in patients with microprolactinoma, acromegaly and nonsecreting adenoma. None of the 6 patients with macroprolactinoma underwent normalization of plasma PRL, but the latter was markedly reduced (61-80% of basal levels). A second injection of the drug in 5 macroprolactinoma patients induced a further reduction of plasma PRL levels in 2 of them. No changes in the tumor size were observed either after the first or the second injection of long-acting bromocriptine in any of the patients. This injectable form of bromocriptine induced nausea and/or mild hypotension lasting a few h in 4 of the 10 patients and was better tolerated than the oral form as regards both the duration and intensity of the side effects. Thus, as this drug has proved to be efficacious and well tolerated by the patients, this long-acting form of bromocriptine may be a valid therapeutical approach for initiating medical treatment of patients with prolactinoma.

Acromegaly↗
PubMedDate not supplied

Bromocriptine acute effect on insulin, glucagon and growth hormone levels in acromegalic patients.

It has been shown that L-dopa or dopamine administration influences glucose metabolism, as well as insulin and glucagon release in man. In the present study, the effect of bromocriptine (CB-154), a long-acting dopamine agonist, on insulin, glucagon and growth hormone secretion in 32 acromegalic patients was investigated. Glucose, insulin and plasma glucagon levels were not modified following administration of bromocriptine or placebo. Moreover, plasma GH levels were decreased by more than 50% in 18 of the 32 acromegalics. Mean GH levels were significantly lower with respect to levels observed following placebo at 60 min to the end of the test (p less than 0.001). Administration of a double dose of CB-154 (5 mg po) one hour before arginine test did not affect insulin or glucagon secretion with respect to levels observed during arginine alone. In addition, there was a fall in GH levels similar to that observed following administration of bromocriptine alone. These findings suggest that bromocriptine in itself does not exert a direct action on insulin and glucagon release. Improvement in glucose tolerance and reduction in insulin secretion observed following prolonged CB-154 treatment in acromegalic patients are probably due to a simultaneous inhibition of GH secretion or to other peripheral effects of bromocriptine.

Acromegaly↗
PubMed1984

Recovery of serum TSH and thyroid hormones after 3'isopropyl-3,5-diiodo-L-thyronine (DIIP) treatment: absence of inhibiting effect of bromocriptine on TSH secretion and evidence for autoregulation of serum T3 levels.

Bromocriptine, because of its dopaminergic activity, could possibly inhibit TSH secretion. This hypothesis was tested in 7 normal male volunteers. Thyroid function was suppressed with the very potent thyromimetic analogue, 3'isopropyl-3,5-diiodo-L-thyronine (DIIP). We wanted to observe, after stopping this treatment, whether the return of serum T3, T4, rT3 and TSH values was influenced by concomitant bromocriptine treatment (5 mg/day). For comparison, the DIIP study was also performed without bromocriptine treatment. In both cases, serum T4 and serum T3, which had decreased by, respectively, 34% +/- 5% and 17% +/- 5%, returned over the same time interval to their initial values. Serum TSH and TRH-mediated TSH secretion were also unaffected by the bromocriptine treatment. DIIP does not interfere in the serum determination of T3, T4 and rT3. During suppression with DIIP serum T3 fell less than serum T4 and returned more rapidly to its initial concentrations. It is concluded that dopaminergic inhibition by bromocriptine, at this dose, is insufficient to alter normal thyroid function. In addition, during suppression and shortly thereafter there is a tendency for the serum T3 levels to be maintained.

Adult↗
PubMedDate not supplied

Effect of bromocriptine administration on gastric acid and gastrin secretion in man.

The effects of acute oral administration of the dopaminergic drug, bromocriptin (5 mg), on basal and submaximal (1 and 3 microgram per kg bw given sc) and maximal (6 mug per kg bw) pentagastrin-stimulated gastric acid secretion and on basal and meal-induced gastrin release have been evaluated in healthy volunteers. Although basal and maximal pentagastrin-stimulated acid output did not change, the response to submaximal pentagastrin doses was significantly increased. Basal and stimulated serum gastrin concentrations were not modified, nor was fasting serum gastrin during chronic bromocriptine treatment (10 mg per day for 90 days) in acromegalic patients. As dopamine infusion is known to reduce basal and pentagastrin-induced gastric acid secretion, the presently reported effect of bromocriptine is not dependent on dopamine receptor stimulation. It is suggested that it might be due to alpha-adrenergic and/or serotoninergic antagonism, both actions being properties of bromocriptine. Alternatively, since bromocriptine, at variance with iv infused dopamine, crosses the blood-brain barrier, the effect of this drug on gastric function might depend on interference by centrally mediated actions on those directly exerted at the gastric level.

Acromegaly↗
PubMedDate not supplied

Long term bromocriptine therapy in Cushing's disease.

Recently, bromocriptine has been successfully introduced as medical therapy for the pituitary hypersecreting syndromes of hyperprolactinemia and acromegaly. Subsequently, an inhibitory effect on ACTH secretion was reported using bromocriptine in Cushing's disease. While most studies have focused on the acute response to bromocriptine, few have investigated the response to chronic therapy with this agent. In this report, we describe a patient with Cushing's disease in whom an acute inhibition of ACTH and cortisol was demonstrated following bromocriptine and in whom the long term administration of bromocriptine as the sole therapy produced a transient beneficial response. Further pharmacologic testing suggested this inhibitory effect on the hypothalamic-pituitary-adrenal axis was mediated through dopaminergic stimulation.

Adrenocorticotropic Hormone↗
PubMed1985

Effect of chronic bromocriptine administration on tumor size in patients with "nonsecreting" pituitary adenomas.

The effect of chronic bromocriptine administration (7.5-20 mg/day for 1-32 months) on the size of "nonsecreting" pituitary adenomas (NPA) was studied in 20 patients. Brain computed tomography showed a marked reduction of the adenoma in one patient after 1 month of treatment (7.5 mg/day); further scans taken 2 and 15 months later, under the same bromocriptine dose, did not show any other variations in the tumoral mass. In the remaining 19 patients, no changes in tumor size were documented by CT during the treatment. Four patients had a worsening of visual fields during bromocriptine administration and they were referred for neurosurgery. In conclusion, bromocriptine was ineffective in reducing tumor size in all but one patient with NPA and, in some cases, it did not prevent tumor growth as is suggested by the worsening of visual fields. Thus, bromocriptine treatment, at least at the doses capable of shrinking macroprolactinomas, seems to be of limited value in patients with NPA.

Adenoma↗
PubMed2002

Effects of amantadine and bromocriptine on startle and sensorimotor gating: parametric studies and cross-species comparisons.

BACKGROUND: We recently reported that prepulse inhibition (PPI) in humans was increased by the dopamine (DA) agonist/ N-methyl- D-aspartate (NMDA) antagonist amantadine (200 mg), but was not significantly altered by the DA agonist bromocriptine (1.25-2.5 mg). PPI-enhancing effects of DA agonists occur in rats under specific stimulus conditions, including short prepulse intervals (<30 ms). We characterized the effects of amantadine and bromocriptine on PPI across species, assessing: (1) dose-response effects on PPI in rats over 10- to 120-ms prepulse intervals; (2) drug effects on PPI in humans, using this same range of prepulse intervals; and (3) drug effects on measures related to PPI, including PPI of perceived stimulus intensity (PPIPSI), and startle habituation. METHODS: Drug effects on PPI were assessed in male Sprague Dawley rats ( n=90) and humans ( n=49); startle habituation and PPIPSI were also studied in humans. RESULTS: Amantadine and bromocriptine exhibited dose- and stimulus-dependent effects on PPI in rats, increasing PPI with short (10-20 ms) prepulse intervals, and decreasing PPI with long (60-120 ms) prepulse intervals. In humans, amantadine increased PPI with both short (20 ms) and long (120 ms) prepulse intervals. Bromocriptine had no significant effect on PPI in humans, but tended to increase PPI at short (20 ms) intervals. Amantadine eliminated PPIPSI. CONCLUSIONS: Amantadine modifies prepulse effects on startle in rats and humans, and disrupts prepulse effects on perceived stimulus intensity in humans; bromocriptine has clear effects on PPI in rats, but not in humans. The divergent effects of amantadine on sensorimotor and sensory effects of prepulses may reflect a divergence of brain circuitry regulating these processes.

Acoustic Stimulation↗
PubMed1983

The effects of bromocriptine in patients with congestive heart failure.

The sympathetic nervous system and the renin-angiotensin system are activated in patients with congestive heart failure (CHF) and could be contributing to excessive peripheral vasoconstriction and impaired myocardial performance. Bromocriptine, an orally active ergot alkaloid with dopaminergic receptor agonist actions, is known to lower plasma norepinephrine in humans. It could also possess direct vasodilator activity through vascular dopaminergic receptors. To assess the effects of bromocriptine on hemodynamic measurements, sympathetic nervous system activity, and the renin-angiotensin system in patients with heart failure, we measured standard hemodynamic parameters and plasma norepinephrine and plasma renin activity before and following a single oral dose of 2.5 mg of bromocriptine in 10 patients with chronic stable heart failure. The following statistically significant (p less than 0.01) peak responses were noted: plasma norepinephrine decreased from a mean +/- 1 SD of 581 +/- 194 to 366 +/- 181 pg/ml; mean heart rate declined from 87 +/- 16 to 78 +/- 17 bpm; mean blood pressure was reduced from 87 +/- 9 to 73 +/- 9 mm Hg; systemic vascular resistance decreased from 1494 +/- 361 to 1249 +/- 289 dynes X sec X cm-5; stroke volume index increased from 27 +/- 7 to 33 +/- 10 ml/beat/M2; left ventricular filling pressure decreased from 28 +/- 8 to 21 +/- 8 mm Hg; and mean right atrial pressure fell from 10 +/- 4 to 7 +/- 4 mm Hg. Plasma renin activity did not change significantly. All patients tolerated the drug well. Although the effects of bromocriptine on plasma norepinephrine may contribute to an improved hemodynamic state, other mechanisms of action are likely. A direct vasodilator effect via vascular dopaminergic receptor stimulation is possible. We conclude that bromocriptine improves the hemodynamic profile in heart failure acutely and that long-term studies are appropriate to better characterize the role of this agent.

Aged↗
PubMed1983

Continuous administration of bromocriptine in the prevention of neurological complications in pregnant women with prolactinomas.

Continuous bromocriptine treatment was given throughout pregnancy to 10 pregnant women with prolactinomas. The dosage of bromocriptine was modified to reduce the serum prolactin level to below 20 ng/ml. Eight patients had continuous bromocriptine treatment started early in their pregnancies, and no tumor-related neurological complications were observed. Continuous bromocriptine treatment was not started at the onset of pregnancy in two patients, and bitemporal hemianopia occurred (at 5 and 7 months of pregnancy). With the start of continuous bromocriptine treatment, a normalization of the visual fields rapidly ensued. The course of the pregnancies and the condition of the newborn infants at birth were normal. The subsequent mental and physical development of the newborn infants (observed up to the age of 6 years) was also normal.

Adult↗
PubMed1985

Hormonal and morphologic effects of bromocriptine on normal rat pituitary and GH3 tumor cells.

Bromocriptine in concentrations up to 5 X 10(-4) mol/L was studied for any deleterious effects upon normal rat pituitary cells, as well as on the rat GH3 cell line. Normal rat pituitary glands were obtained by decapitation from 50-day-old female Wistar rats and dispersed with 0.25% trypsin. The cells (10(5) per plate) were then incubated in 60 by 15 mm plates (Falcon) that contained 3 ml of Dulbecco's modified Eagle's medium with 10% fetal calf serum. GH3 cells were plated in a similar fashion. Bromocriptine was added in concentrations of 5 X 10(-4) to 5 X 10(-9) mol/L, and aliquots of medium were obtained at 6, 24, and 48 hours for the determination of growth hormone and prolactin. Cell counts were performed at 24 and 48 hours. A significant reduction in concentrations of growth hormone and prolactin was observed with concentrations of bromocriptine of 5 X 10(-5) and 5 X 10(-4) mol/L at 24 and 48 hours (p less than 001). Although no significant changes in cell counts were observed in the normal rat pituitary cells, the GH3 cells showed complete disruption at 48 hours only in the plates that contained the highest concentrations of bromocriptine. Electron microscopy of normal rat cells and GH3 demonstrated selective cytotoxic effects only on the GH3 cells. In conclusion, bromocriptine has been demonstrated to have a direct effect on hormone release and on the morphologic characteristics of tumor cells but not normal pituitary cells.

Animals↗
PubMed1990

Bromocriptine as an adjuvant to cyclosporine immunosuppression after heart transplantation.

Prolactin, a pituitary hormone, has been shown to have an active role in the regulation of the immune system. Prolactin receptors have been described on the membrane of lymphocyte cells, and competitive binding to these receptors by cyclosporine and circulating prolactin has been demonstrated. Experimental evidence suggests a synergistic effect of cyclosporine and bromocriptine, an inhibitor of pituitary release of prolactin, on immunosuppression. Between July 1986 and January 1988, 54 patients were randomly assigned to two groups of immunosuppression treatment. Thirty patients (group 1) were administered cyclosporine, azathioprine, and prednisone and 24 patients (group 2), a modified protocol aimed at decreasing the level of circulating prolactin by adding bromocriptine to the immunosuppression regimen. The two groups were similar in regard to age, preoperative diagnosis, and duration of follow-up. Minimal side effects related to bromocriptine were observed. The overall incidences of rejection and infection were similar, although actuarial analysis showed that freedom from these complications among patients treated with bromocriptine was significantly higher throughout the first 2 months after heart transplantation compared with that of patients in the control group. Other variables such as serum cyclosporine levels and lymphocyte counts were similar in both groups. In conclusion, suppression of circulating prolactin by bromocriptine appears to improve the immunosuppressive effect of cyclosporine, at least during the early postoperative period when the risk of rejection and infection is higher, and could be a promising avenue to successful hormonal manipulations of the immune process after organ transplantation.

Actuarial Analysis↗
PubMed1996

Effects of bromocriptine and/or L-DOPA on neurons in substantia nigra of MPTP-treated C57BL/6 mice.

The effects of bromocriptine and/or L-DOPA on substantia nigra neurons of MPTP-intoxicated mice were investigated. L-DOPA reduced the number of neurons. Bromocriptine protected the neurons from damage by L-DOPA but had no effect on the neurons damaged by MPTP. The treatment of bromocriptine and L-DOPA protected the neurons compared with single administration of bromocriptine. It seems reasonable to suppose that bromocriptine should be added to L-DOPA in order to protect the neurons in parkinsonism.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMedDate not supplied

Bromocriptine for "negative" schizophrenia.

The hypothesis that the pathophysiology of negative symptoms in schizophrenia may involve relative hypoactivity of central dopaminergic neurotransmission prompts the exploration of dopamine agonist strategies in the treatment of this condition. Although the use of dopamine agonists in otherwise unmedicated schizophrenic patients often leads to the exacerbation of psychosis, trials of dopamine agonists in combination with neuroleptic agents warrant investigation. We therefore report on open clinical experience involving six patients with chronic negative symptoms of schizophrenia, maintained on neuroleptic medication, who appeared to have favorable responses to the addition of moderate doses of bromocriptine (10 to 20 mg/d orally in divided doses). One particular factor that makes these trials potentially informative is that five of the six patients had failed to respond to standard treatments with anticholinergic antiparkinsonian medication before the bromocriptine trial, making it unlikely that the bromocriptine had its effect purely by counteracting neuroleptic-induced akinesia. A trial of bromocriptine under these circumstances has never been reported. A second unique feature of this report concerns the lengthy period of follow-up. Adjunctive bromocriptine was continued for a total of 27 patient-years in the six individuals, with maintenance of favorable course and minimal incidence of psychotic exacerbation.

Activities of Daily Living↗
PubMed1990

Effects of chronic treatment of MPTP monkeys with bromocriptine alone or in combination with SKF 38393.

Eight monkeys developed a severe parkinsonian syndrome after i.v. administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Treatment with bromocriptine (5 mg/kg) relieved the parkinsonian symptoms, but the efficacy of this treatment appeared to decrease slightly with time. The addition of SKF38393 (5 mg/kg) to the bromocriptine treatment in four monkeys prevented and even reversed the tendency to decreased efficacy with an increased response in three out of four animals. Neither of these two treatments induced dyskinesia in these monkeys. Dopamine D1 and D2 receptors, assayed in the caudate nucleus, the putamen and nucleus accumbens with [3H]SCH 23390 and [3H]spiperone binding respectively, were not significantly different in MPTP monkeys treated with bromocriptine or with bromocriptine plus SKF38393. Monkeys in the two treatment groups had a similar extent of denervation of the striatum and accumbens as assessed by the content of dopamine and its metabolites. These results suggest that in MPTP monkeys, the behavioral response to the D2 agonist bromocriptine can be enhanced by concomitant activation of the D1 receptors while this combination of agonists does not induce dyskinesia. The addition of the D1 agonist does not appear to cause further alteration of the D1 or D2 receptors.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1985

Immunofluorescence demonstration of tubulin and actin in estrogen-induced rat prolactinoma cells in vitro. Alteration of their distribution after bromocriptine, colchicine and cytochalasin B treatments.

Cultured cells in vitro from estrogen-induced rat prolactin-secreting adenomas (prolactinomas) were examined by indirect immunofluorescence microscopy for the distribution of cytoskeletal proteins and alterations of cytoskeleton after treatment with bromocriptine, colchicine and cytochalasin B (CB). After 8 days in culture, prolactinoma cells were well expanded and developed cytoplasmic processes were seen. The cytoplasmic microtubules were observed as fine reticular networks radiating from perinuclear portions toward the cell periphery when decorated with an antibody against tubulin. On the other hand, the actin filaments showed diffuse and spotty distribution when detected with an anti-actin antibody. Contaminated fibroblasts showed a reticular distribution of microtubules and a parallel array of actin cables which corresponds to "stress fibers" throughout the cytoplasm. After treatment with bromocriptine, the reticular distribution of microtubules in prolactinoma cells changed into a coarse and sparse pattern, which was identical with the changes in the distribution of tubulin after treatment with colchicine. On the other hand, distribution of actin was not affected by bromocriptine. Bromocriptine treatment did not alter the distribution of microtubules and actin filaments in fibroblasts, whereas colchicine changed the distribution of microtubules in both prolactinoma cells and fibroblasts. CB treatment changed the localization of actin filaments in both kinds of cells. These in vitro studies indicated bromocriptine would selectively affect the cytoplasmic microtubular system of prolactinoma cells.

Actins↗
PubMed1986

Effects of hypersecretion of growth hormone and prolactin on plasma levels of glucagon and insulin in GH3-cell-tumor-bearing rats, and the influence of bromocriptine treatment.

Plasma levels of prolactin, growth hormone, glucagon insulin and glucose were measured in non-treated control rats, bromocriptine-treated control rats and GH3-cell-tumor-bearing rats with and without bromocriptine treatment. Bromocriptine treatment increased plasma levels of glucagon, insulin and glucose in control rats. Tumor-bearing rats had increased body weight and increased plasma levels of prolactin, growth hormone, glucagon, insulin and glucose. Bromocriptine treatment reduced body weight and decreased the plasma levels of prolactin, glucagon and insulin, as compared to non-treated tumor-bearing rats. The drug had no effect on plasma levels of growth hormone and glucose. These results indicate that, in GH3-cell-tumor-bearing rats, prolactin, glucagon and insulin are more sensitive to the action of bromocriptine than growth hormone.

Animals↗