Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Bromocriptine”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 649 records · Page 36Linked to original sources

A preliminary study of the ocular hypotensive effects of bromocriptine in diabetic patients with autonomic neuropathy.

The effect of bromocriptine on intraocular pressure has been investigated in a group of 8 diabetic patients with autonomic neuropathy, to test the hypothesis that bromocriptine exerts its ocular hypotensive action through presynaptic dopamine receptors. Bromocriptine eye drops (0.025%) produced a significant fall in intraocular pressure in a control group of 8 matched normal volunteers, but this effect was not seen in the eyes of the diabetic patients. These results are consistent with a presynaptic site of action of bromocriptine.

Adult↗

Treatment of pseudopregnancy with bromocriptin, an ergot alkaloid.

One hundred and forty-two dogs with single or multiple pseudopregnancies were treated with bromocriptin at three different dose rates and once in combination with mobilerone. The treatments that scored best were 30 micrograms/kg bromocriptin for 16 days and 10 micrograms/kg bromocriptin for 10 days. Vomiting was a frequent side effect (about 20 per cent of cases) and was treated successfully with metoclopramide at a dosage of 0.5 mg/kg. Metoclopramide had no effect on the effectiveness of the bromocriptin.

Animals↗

Pituitary adenomas: possible role of bromocriptine in intratumoral hemorrhage.

Magnetic resonance (MR) images of 68 patients examined for adenomas of the pituitary gland were retrospectively reviewed for the presence of hyperintensity on T1-weighted images because of recent reports suggesting that bromocriptine treatment may affect T1 values. Twenty-seven patients were examined after either surgery or radiation therapy, 29 were receiving bromocriptine, and 22 had not received any treatment at the time of MR imaging. MR imaging criteria showed evidence of subacute or chronic intratumoral hemorrhage in 18 patients, five of whom had hemorrhage proved at surgery. Ten of the 18 patients were asymptomatic from the hemorrhage; eight had headaches, visual field cuts, or cranial nerve deficits. Although an increased frequency of intratumoral hemorrhage was noted in prolactinomas and macroadenomas and in patients undergoing bromocriptine therapy, the effect of bromocriptine on bleeding was the only significant correlation (P less than .01).

Adenoma↗

Late development of resistance to bromocriptine in a patient with macroprolactinoma.

We report the case of a man with an invasive macroprolactinoma who developed resistance to bromocriptine to which he had previously responded satisfactorily for 5 years. Subsequently, hyperprolactinemia was controlled equally well with 600 microg quinagolide daily and later with 4.5 mg cabergoline weekly. This observation suggests that a loss of dopamine receptors at the tumoral cell surface might be the mechanism underlying acquired resistance to bromocriptine. In addition, no tumor growth was observed over a 10-year follow-up, which virtually excludes a malignant transformation of the prolactinoma. This case emphasizes the need for close supervision of patients with macroprolactinoma, even after the serum prolactin concentration has been normalized by bromocriptine. It furthermore illustrates the usefulness of quinagolide and cabergoline when resistance to bromocriptine develops after a prolonged period of adequate response to this drug.

Aminoquinolines↗

Bromocriptine combined with levodopa in Parkinson's disease.

Bromocriptine (Parlodel) was given for 2 years to 17 parkinsonian patients showing inadequate response to treatment over a mean of 7 years with levodopa combined with a decarboxylase inhibitor. 11 of the patients had developed dyskinesia and 13 the on-off phenomenon during levodopa therapy. When the dose of bromocriptine reached 30 mg daily, after 4 weeks' treatment, a highly significant improvement (p less than 0.001) was observed in the following six variables: bradykinesia, rigidity, tremor, feeding, dressing and speech. These improvements have now been maintained for 2 years. The on-off phenomenon disappeared in 9 out of 13 patients. Side effects were mild and transient. Involuntary movements existing prior to bromocriptine administration were improved by reducing the dose of levodopa. The mean daily dose--after progressive and individual adjustment--was 46 mg bromocriptine combined with 435 mg levodopa plus decarboxylase inhibitor.

Aged↗

Second interim report of the nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients.

The interim data obtained up to the end of the 2nd year of the nation-wide multicentric cooperative study on the long-term effects of bromocriptine in parkinsonian patients revealed the following results. Firstly, the bromocriptine monotherapy could be continued in about 40% of the patients at the mean maintenance dose of 10.8 mg daily. Secondly, the additional use of bromocriptine in parkinsonian patients already treated with levodopa had a favorable influence on late side effects of levodopa such as on-off phenomenon and dyskinesia. No significant difference has been found so far as to the management of the wearing-off phenomenon between the patients with levodopa alone and those with levodopa and bromocriptine.

Adult↗

Third interim report of the nationwide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients.

The interim results obtained up to the end of the 3rd year of the multicenter nationwide cooperative study on the long-term effects of bromocriptine in parkinsonian patients are reported. Bromocriptine monotherapy could be continued in approximately 33% of the patients at the mean maintenance dose of 11.4 mg/day. The combined use of bromocriptine (11.1 mg/day) in parkinsonian patients already treated with levodopa had a favorable influence on the long-term side effects of levodopa such as the on-off phenomenon and dyskinesia. The beneficial effects of bromocriptine, levodopa and an early combination on parkinsonian symptoms such as rigidity and tremor remained at the end of the 3rd year. However, the effects of each mode of therapy on another parkinsonian symptom, akinesia, ceased by the end of the 3rd year.

Adult↗

Bromocriptine therapy in early-stage Parkinson's disease.

We evaluated bromocriptine monotherapy during the early stage of Parkinson's disease (Hoehn and Yahr stage I or II). Of the 120 patients registered as participants in this trial, 96 were studied. The follow-up period was 48 weeks. For the first 24 weeks they were all placed on bromocriptine with or without anticholinergic drugs; for the second 24 weeks, 75 of them were still kept on the same medication, with 21 requiring additional levodopa. Clinically, the former group showed a good response to the bromocriptine monotherapy, while the latter responded poorly to it (requiring in addition levodopa). We think that Parkinson's disease encompasses a heterogeneous group of patients of whom about 75% are well treated by bromocriptine alone at the early stages of the illness.

Antiparkinson Agents↗

Apoptosis in the anterior pituitary gland of the rat: studies with estrogen and bromocriptine.

Apoptosis was investigated by electron and light microscopy in the anterior pituitary gland of the male Fischer rat in which hyperplasia of prolactin-secreting cells had been induced by estrogen implanted subcutaneously for 6 weeks. Counts by light microscopy of apoptotic cells and cells containing phagocytosed apoptotic bodies increased during a period of 44 h after estrogen withdrawal. Necrosis was present but was not prominent. Administration of bromocriptine after estrogen withdrawal increased apoptotic counts to nearly double those in the absence of bromocriptine. Bromocriptine caused some increase in necrosis. Apoptosis occurred in prolactin-secreting cells identified by immunostaining and in other cells. Phagocytosed apoptotic bodies were seen in folliculo-stellate and not in other cells. It is concluded that apoptosis occurs in the anterior pituitary gland and is induced by bromocriptine. Phagocytosis of apoptotic bodies is a function of the folliculo-stellate cells.

Animals↗

Stimulation of "regulatory" dopamine receptors by bromocriptine (CB-154).

Bromocriptine produces long-lasting hypomotility and decreases brain dihydroxyphenylacetic acid (DOPAC) in mice. These effects are obtained with doses much lower than those which produce hypermotility. The decrease of brain DOPAC is correlated to the hypomotility both on a dose and on a time basis. Potent DA receptor blockers as pimozide, benzperidol and droperidol antagonize the hypomotility and the decrease of brain DOPAC produced by bromocriptine. These effects are obtained with very low doses (0.05-0.3 mg/kg) of neuroleptics which per se do not affect motility or brain DOPAC. The maximal decrease of brain DOPAC produced by bromocriptine is similar to that produced by apomorphine and the combination of these drugs does not result in a further decrease. On the basis of these results it is postulated that bromocriptine decreases DA turnover and produces hypomotility by acting on "regulatory" DA receptors different from the postsynaptic ones of the "terminal" dopaminergic areas.

3,4-Dihydroxyphenylacetic Acid↗

Effect of bromocriptine on acetylcholine output from the cerebral cortex.

The effect of bromocriptine on acetylcholine (ACh) output from the cerebral cortex was investigated in anaesthetized rats. Bromocriptine caused a brief decrease in ACh output at the dose of 0.1 mg/kg i.p. and a dose-related long-lasting increase at doses from 1.25 to 10 mg/kg i.p. Apomorphine elicited an increase in ACh output when injected intraperitoneally at doses from 0.1 to 10 mg/kg. When bromocriptine was administered to rats in which a septal lesion had been made 12 days prior to the test, no increase in ACh output was observed. Bromocriptine seems therefore to stimulate a cortical cholinergic pathway originating from or passing through the septum.

Acetylcholine↗

Bromocriptine and hydergine: a comparison on striatal or hypothalamic adenylate cyclase activity.

We compared the effects of bromocriptine and of hydergine on striatal and hypothalamic adenylate cyclase activity. Rats treated with bromocriptine (5 mg/kg) or with hydergine (3 mg/kg), showed a stimulation of adenylate cyclase activity in the striatum, but not in the hypothalamus. Furthermore, we considered the competitive action bromocriptine and hydergine had on the dopamine-stimulating effect of the adenylate cyclase activity. There was a definite inhibition of the dopamine-stimulating effect both in the striatum and in the hypothalamus of the rats treated with bromocriptine. In those treated with hydergine we observed an inhibiting effect on the striatum and an increased dopamine stimulation on the hypothalamus.

Adenylyl Cyclases↗

Gel filtration studies of serum growth hormone in acromegaly following bromocriptine administration.

Sera of 7 patients with active acromegaly were fractionated by Sephadex G-100 chromatography and the effects of bromocriptine on the concentrations of total growth hormone (hGH) and its different molecular forms studied. Three immunoreactive peaks were observed, corresponding to molecular weights of about 20,000 ('little hGH'), 40,000 ('big hGH'), and more than 100,000 ('big big hGH') Following bromocriptine administration, there was significantly more reduction of 'little hGH' than of 'big big hGH'. Careful interpretation of these changes is required in view of the possible influences of sample storage and handling on hGH heterogeneity. We suggest that either bromocriptine acts differentially on the release of 'little' and 'big big hGH', or that these components differ in their metabolic half-life. However, even the suppression of 'little hGH' is insufficient to explain the clinical response of the disease to bromocriptine.

Acromegaly↗

Restoration of normal gonadotropin responses to naloxone by chronic bromocriptine treatment in elderly men.

Naloxone is unable to stimulate FSH and LH secretion in elderly men, suggesting a reduced endogenous opioid control of gonadotropin secretion in senescence. In the present study, we examined whether in elderly men a chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days) modifies the gonadotropin response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h). Eleven younger men (group 1, 22-40 years old) participated as controls. Twenty-two elderly men were selected from a larger population and were divided into two groups: subjects with compensated gonadal failure (normal blood testosterone and elevated gonadotropin concentrations; group 2, n = 11; 62-80 years old) and men with normal gonadal function (normal blood testosterone and gonadotropin levels; group 3, n = 11; 61-82 years old). Naloxone induced a striking LH and a slight but significant FSH increase in group 1, but was unable to change serum gonadotropin concentrations in elderly subjects of both groups 2 and 3. When experiments were repeated after bromocriptine treatment, no significant differences in LH and FSH responses to naloxone were observed in the younger subjects. On the other hand, bromocriptine restored significant gonadotropin responses to naloxone in elderly men. In fact, after bromocriptine, naloxone-induced FSH and LH increments in groups 2 and 3 were indistinguishable from those observed in group 1. These data suggest that in men age-related dopaminergic alterations may underlie the defective endogenous opioid control of gonadotropin secretion.

Adult↗

Puerperal lactation, gonadotropin release and estradiol release: effects of metergoline and bromocriptine.

The exact cause of amenorrhea during the puerperium is still a matter of debate. PRL might inhibit primarily the release of FSH and LH or their stimulating effects on the ovary. In the study presented here, 28 healthy women were investigated, 13 of them lactating puerperae. In the other 15, lactation was prevented by drugs (metergoline in 9, bromocriptine in 6). The women's serum PRL, FSH, LH, beta-HCG and 17 beta-estradiol as well as their FSH and LH response to LHRH (100 micrograms i.v.) were tested 1, 3, 7 and 14 days after vaginal delivery. Serum PRL levels remained elevated in the lactating puerperae and dropped in the puerperae treated with metergoline or bromocriptine. The pattern of FSH, LH and beta-HCG levels as well as the FSH and LH response to LHRH were superimposable in lactating and in nonlactating women. 17 beta-estradiol levels dropped in all puerperae from day 1 to 7, but rose from day 7 to 14 only in the puerperae treated with metergoline or bromocriptine and not in the lactating women. These data indicate that PRL directly affects the ovarian response to FSH and LH, whereas the release of FSH and LH remains unaffected. A stimulatory effect of metergoline and bromocriptine on the ovarian steroidogenesis cannot be excluded.

Adult↗

No effects of l-dopa and bromocriptine on psychophysiological parameters of human selective attention.

Patients with schizophrenia exhibit diverse cognitive deficits, one of which is a loss of the ability to focus attention. According to the revised dopamine hypothesis of schizophrenia both an increased mesolimbic and a decreased prefrontal dopaminergic activity is suggested to be involved in schizophrenia. The current study was designed to explore the relationship between dopamine and two psychophysiological parameters of selective attention, i.e. P300 amplitude and processing negativity (PN) in healthy volunteers. In two separate experiments, with a double-blind, balanced and placebo-controlled crossover design, 18 healthy male volunteers were orally administered either 300 mg l-dopa (precursor of dopamine) or placebo (experiment I), or 1.25mg bromocriptine (D2 agonist) or placebo (experiment II). Following this treatment they were tested in an auditory, dichotic selective attention paradigm. An increase in P300 amplitude was found following deviant stimuli when compared to standard stimuli and following attended stimuli when compared to unattended stimuli, regardless of treatment. Similarly, PN was found regardless of treatment. Neither l-dopa nor bromocriptine affected task performance or the amplitudes of PN or P300. In the present study neither l-dopa nor bromocriptine affected PN, P300 amplitude or task performance in healthy controls, phenomena which are usually found to be disrupted in schizophrenia. This indicates that P300 amplitude and PN are neither affected by a global (l-dopa) increased dopaminergic activity, nor by a more selectively towards striatal areas targeted (bromocriptine) increase in dopaminergic activity.

Adult↗

Effects of L-dopa and bromocriptine on calcitonin secretion in medullary thyroid carcinoma.

The secretion of calcitonin (CT) by thyroid C cells has been reported to be reduced by dopamine in vitro and by L-dopa in patients with medullary thyroid carcinoma (MTC). These results have suggested that dopa uptake ad decarboxylation to dopamine may play an inhibitory role in the control of CT secretion. We studied the effects of either L-dopa or bromocriptine, a dopamine agonist, on CT secretion in 11 patients with MTC. Seven patients had multiple endocrine adenomatosis type II (MEA II), 1 had MEA III, and 3 had sporadic MTC. Metastatic disease was confirmed in 8, was probable in 2, and was absent in 1. L-Dopa (500 mg orally) was given to 10 patients in 12 trials. Serum obtained serially for CT measurement RIA over a 4-h period showed a fall in 4 instances in 3 patients; there was no decrease in 7 patients. Absorption of L-dopa was confirmed by the finding of the expected rise in serum GH concentration in all nonresponders except 1. Bromocriptine administered in increasing doses (7.5-50 mg/day) for periods from 4-18 weeks in 5 patients with metastatic disease failed to lower the serum CT concentration in any patient. In 2 of 4 cases, pentagastrin-induced CT release was augmented during bromocriptine administration. These results show L-dopa suppression of CT secretion only in a minority of patients with MTC; the lack of response to bromocriptine suggessts that dopamine receptor stimulation by dopaminergic ergots does not inhibit CT secretion in this same group of patients.

Adolescent↗

Failure of bromocriptine to lower plasma catecholamines in normal men and women.

A plasma catecholamine-lowering effect of bromocriptine has previously been reported in normals, but not in patients with PRL- or GH-secreting pituitary tumors, and has been used as evidence to support the concept of disordered central nervous system dopaminergic tone in patients with such tumors and as a test to distinguish them from normals. In the present study of 16 normal subjects (9 women and 7 men), we found no significant change in plasma norepinephrine or epinephrine after bromocriptine. Similarly, no change occurred in plasma catecholamines in 8 patients with PRL-secreting tumors or 6 patients with ACTH hypersecretion. Our data, therefore, do not provide confirmatory evidence for an effect of bromocriptine on plasma catecholamines in normal subjects and do not support the proposed use of bromocriptine as a test for defective central dopaminergic regulation.

Adrenocorticotropic Hormone↗