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PubMedDate not supplied

Effect of prolactin and bromocriptine administration on epididymal function--a biochemical study in rats.

The pattern of androgen dependent enzyme activities of epididymis was studied after the administration of prolactin and bromocriptine in albino rats. Prolactin activated the glycogenolysis and hexose mono and diphosphate pathways, which would be essential for sperm maturation. But bromocriptine inhibited these activities of epididymis. Hence role of bromocriptine in decreasing epididymal function has been suggested.

Animals↗
PubMed1986

Inhibition of lactation by a long-acting bromocriptine.

A long-acting form of bromocriptine, a prolactin (PRL) secretion inhibitor, was administered to 122 postpartum women in single intramuscular injections of 20 (N = 24), 30 (N = 22), 40 (N = 46), and 50 mg (N = 30). In 91 women the substance was administered immediately after delivery to prevent galactopoiesis and in the remaining 31 women to inhibit established lactation. Effectiveness was estimated by the absence of breast engorgement and of milk secretion. Successful prevention or inhibition of lactation was highest among women receiving 50 mg bromocriptine (97%), and comparison between dosages revealed a close linear dose-response relationship (r = 0.98). Persistent and significant (P less than .001) PRL inhibition could be recorded for up to 22 days in successfully treated puerperas in comparison with 12 normally breast-feeding women who served as control subjects. No significant side effects or local reactions were recorded. Eleven of 46 postpartum women receiving 20 or 30 mg bromocriptine experienced onset of milk secretion or lactation rebound, and responded to oral administration of the drug. The presence of milk was associated with plasma PRL concentrations persistently above 25 ng/mL in all of them, whereas nine women in the same dosage range in whom lactation suppression was effective exhibited values below this limit. Dose-response data allow the establishment of a putative PRL threshold for induction of milk secretion of about 25 ng/mL. Maintenance of plasma PRL values below this limit prevents lactogenesis and inhibits lactopoiesis.

Bromocriptine↗
PubMed1979

Bromocriptine in hyperprolactinemic amenorrhea: a possible early effect on ovarian steroidogenesis.

The effect of bromocriptine was studied in a 28-year-old cretin woman who presented with long-term untreated primary hypothyroidism, primary amenorrhea, hyperprolactinemia, and an enlarged pituitary fossa. Bromocriptine therapy lowered the plasma prolactin and caused an early rise in plasma 17 beta-estradiol levels and uterine bleeding, despite the failure of plasma gonadotrophins to respond to luteinizing hormone release hormone (LHRH) administration. Thus, it is suggested that bromocriptine may have an early direct effect on the ovary in hyperprolactinemic amenorrhea.

Adult↗
PubMedDate not supplied

[Early and late inhibition of lactation using bromocriptine. A comparative study (author's transl)].

After having reviewed our present knowledge of the pharmacology of bromocriptine, its action on the pituitary, centrally and peripherally, the authors detail the results they have obtained in inhibiting lactation in two groups of patients who had delivered normally or had Caesarean sections. In the first group where bromocriptine was started in the first 24 hours with dosages of 2.5 mg every 12 hours for 14 days, clinical signs of breast engorgement and of milk secretion were insignificant and the level of prolactin had dropped to normal menstrual cycle levels from the third day after delivery. In the second group where the first dose of bromocriptine was given at least 48 hours after Caesarean section, the levels of prolactin dropped just as sharply from the third day after delivery, but on the other hand the clinical signs of breast engorgement and milk secretion were marked and completely comparable to those which are found in patients who are not going to breast feed but who have received no treatment to inhibit lactation.

Brain Chemistry↗
PubMed1977

Chromosomal patterns of children born after induction of ovulation with bromocriptine.

We investigated a possible influence of 2-bromo-alpha-ergocryptine (bromocriptine, CB 154) on the human foetus. The chromosome patterns of the children born to mothers treated with bromocriptine before conception and in early pregnancy were examined. In 19 children no numerical or structural chromosomal anomalies which might be ascribed to the use of bromocriptine could be demonstrated.

Bromocriptine↗
PubMed1984

Bromocriptine response in normoprolactinemic patients with polycystic ovary disease: a preliminary report.

Recent work has suggested that a central deficiency or defect of dopamine may contribute significantly to the inappropriate gonadotropin secretion commonly associated with polycystic ovary disease. To evaluate this hypothesis, 2.5 to 5 mg of the dopamine agonist bromocriptine was administered daily to patients with polycystic ovary disease. Prolactin (PRL) levels were normal in all cases and there was no evidence of galactorrhea. All patients had failed to conceive while on clomiphene citrate. Seven patients were treated for a total of nine cycles. Ovulation occurred in four cycles, and two of these patients conceived. In five cycles, no ovulation occurred. Among ovulatory cycles, PRL levels declined, but not to undetectable levels. There was also a periovulatory drop in dehydroepiandrosterone sulfate. Levels of luteinizing hormones rose initially and then dropped to below baseline postovulation. Among anovulatory cycles, PRL fell to undetectable levels and dehydroepiandrosterone sulfate was unaffected. Luteinizing hormone levels rose initially and then dropped slightly. In both ovulatory and anovulatory cycles, follicle-stimulating hormone (FSH) levels remained low. These preliminary data suggest: 1) bromocriptine appears capable of altering gonadotropin secretion in polycystic ovary disease, and 2) variable results on ovulation in polycystic ovary disease may reflect the diverse etiology of the pathophysiology of polycystic ovary disease and/or choosing inappropriate dosages of bromocriptine.

Adult↗
PubMed1984

[Pleuropulmonary fibrosis and bromocriptine].

From a personal case and a review of the literature, it is recalled that bromocriptine may induce pleuropulmonary fibrosis. The various presentations of this condition are described. The index patient is a 56-year-old man, with Parkinson disease and a negative history for respiratory disease, who was taking bromocriptine in a high dose (60 mg/d). Under this treatment, he exhibited weight loss and an inflammatory syndrome and developed interstitial pneumopathy with secondary pleuropulmonary fibrosis, which resolved in part once therapy was discontinued. Bromocriptine, which is an ergot alcaloid with dopaminergic properties, has been used since 1965 in therapy. Its indications, which at the outset were restricted to endocrinology, were extended in 1972 to Parkinson disease, with a significant increase in dosages from 1979. Its responsibility in pleuropulmonary fibroses was suspected in 1981 by Rinne on data from 5 patients. As of now, 8 cases have been reported. All are Parkinson patients who, after a variable time interval (15 days to 3 years), developed a uniform picture of pleuropulmonary disease with rapidly increasing dyspnea upon exertion and deterioration of general health. These features mirror inflammation then fibrosis of the pleura and lung tissue, which results in a variable degree of chronic restrictive respiratory failure. The course is equally uniform, with partial resolution under corticosteroid therapy and more or less significant residual fibrosis at discontinuation of treatment. Immunoallergic rather than toxic or vasomotor mechanisms seem involved.(ABSTRACT TRUNCATED AT 250 WORDS)

Bromocriptine↗
PubMed1984

[Possible effect of bromocriptine on the insulin receptor].

The administration of 0.00011 mg/g weight/day of bromocriptine (CB154) for 7 days to Wistar rats, improved the peripheral glucose uptake without significant changes in plasma insulin level, during the intravenous glucose tolerance test (0.33 g/kg). The mode of the bromocriptine action on binding of 125I insulin to erythrocyte insulin receptors has been evaluated. The total number of sites was greater with bromocriptine (513.1 +/- 124.1 pM/1,CB154 815.6 +/- 107.9 pM/l) (p less than 0.01). The high affinity/low capacity compound of insulin receptor, in CB154 rats (51.8 +/- 16.8 pM/l) was higher than in normal rats (18.3 +/- 8.9 pM/l) (p less than 0.005). Additional studies indicated that CB154 had no effect on the rate of association and dissociation of 125I insulin from rats erythrocyte insulin receptors. The degradation of insulin or the erythrocyte receptor sites do not change, after the treatment with CB154.

Animals↗
PubMed1984

Dopamine receptors: effects of chronic L-dopa and bromocriptine treatment in an animal model of Parkinson's disease.

Male albino rats received a stereotaxic injection of 6-hydroxydopamine (6-OHDA) into the right substantia nigra. Animals demonstrating contralateral rotations 2 weeks postoperatively with apomorphine (0.5 mg/kg i.p.) were treated with L-Dopa (55 mg/kg i.p.), bromocriptine (2 mg/kg i.p.), or polyethylene glycol (vehicle) every 12 h for 30 days. Striatal dopamine (DA) receptors were analyzed by Scatchard plot using 3H-spiroperidol (3H-SP) as ligand. 3,4-Dihydroxyphenylacetic acid (DOPAC) and DA were measured by use of high pressure liquid chromatography. 6-OHDA lesions produced a supersensitivity in striatal DA receptors. Chronic L-Dopa or bromocriptine treatment reversed this supersensitivity. Neither lesion nor drug treatment alone or together produced a significant change in affinity (KD) for 3H-SP. Drug treatment alone also had no effect on Bmax. DA and DOPAC levels were reduced by greater than 98% in lesioned striata. Neither drug treatment affected DA or DOPAC levels as compared with controls. These results indicate that chronic administration of either bromocriptine or L-Dopa will reverse the DA receptor denervation supersensitivity in striatum seen following 6-OHDA lesion. This reversal may play a role in the clinical changes seen in Parkinson's disease patients following chronic use of these drugs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

[Cessation of cerebrospinal fluid rhinorrhea by bromocriptine treatment of a patient with invasive prolactinoma].

As an unusual complication of bromocriptine treatment for prolactinoma, CSF rhinorrhea has been reported in the relevant literature. The authors, on the contrary, experienced cessation of CSF rhinorrhea during bromocriptine treatment. A 37-year-old man with invasive prolactinoma underwent a frontal craniotomy for removal of pituitary adenoma on February 2, 1978. Postoperative CT showed residual adenoma within the sella and the sphenoid sinus. Postoperative irradiation was started on February 27 and given in a total dose of 5,000 rad. On March 30, 1979, the patient noticed clear fluid dropping out of his nostrils, the fluid contained glucose and CSF rhinorrhea was suspected. The CSF rhinorrhea was considered due to the regrowth of adenoma in the paranasal sinuses. On June 27, 1979, the patient developed headache together with fever and CSF rhinorrhea. On examination, the patient was drowsy and showed marked nucheal rigidity. Under the diagnosis of meningitis caused by CSF rhinorrhea antiseptic chemotherapy was started. Hypocycloidal tomogram showed extensive destruction of the sella and a soft density mass in the sphenoid and the ethmoid sinuses. CT also showed intrasphenoidal and lateral extension of the adenoma. To repair of the CSF leak, transsphenoidal surgery was performed on August 2, 1979 when the patient was in favorable condition. The sphenoid sinus was full of adenoma and it was removed, however, the exact location of the CSF leak could not be identified. The sphenoid sinus was packed with muscle tissue. Bromocriptine treatment was postoperatively started with 5 mg per day on August 25, 1979. The patient sustained CSF rhinorrhea which was decreased by lumbar drainage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1981

The extracerebral dopamine antagonist domperidone block the suppressive effect of bromocriptine on prolactin and TSH secretion in man.

The effects of a single oral dose of 2.5 mg bromocriptine on serum level of TSH and prolactin were studied in a group of normal male subjects. Bromocriptine effectively inhibited basal TSH and prolactin concentration as well as the prolactin and TSH response to TRH given 4 hours later. The prior administration of the extracerebral dopamine antagonist domperidone reversed the endocrine effects of bromocriptine. The results suggest that dopamine receptors located at the pituitary may regulate TSH (and prolactin) release in man.

Adult↗
PubMed1982

Hypothalamic-pituitary function following bromocriptine therapy in patients with prolactinomas.

Bromocriptine in a dose of 5 mg daily was given to 18 patients with prolactinomas to promote resumption of menses, to overcome infertility and as a primary treatment for the tumor. Serum prolactin levels fell to within the normal range in 95% of the patients by 12 weeks of therapy. The prolactin response to TRH stimulation was significantly less than before treatment; however, the percent maximum increment was significantly higher. There was no significant change in pituitary reserve of the other hormones. Seven pregnancies occurred during treatment. All the pregnancies have been progressing normally. All patients have already been delivered of healthy babies, including one set of twins. It is suggested that follow-up studies of the various pituitary hormones be conducted on patients on maintenance bromocriptine treatment. In addition, bromocriptine treatment might be used to promote fertility in patients with prolactin-secreting microadenomas.

Adenoma↗
PubMed1983

[The influence of bromocriptine-induced pregnancy and delivery on infertile cases with pituitary microadenoma].

Two consecutive pregnancies were induced in three hyperprolactinemic primary infertile patients bearing intrasellar microadenoma without visual disturbance. Pretreatment prolactin levels, 224 -496ng/ml, were normalized by 10-22.5mg/day of bromocriptine and the initial conceptions occurred. No abnormal sign due to pituitary enlargement was detected throughout the period of gestation and they delivered single full-term babies. Since no significant change was observed in puerperium, it was decided to give the second bromocriptine therapy. The prolactin levels, 80-190ng/ml, measured before the second therapy were apparently lower than those seen prior to the first therapy and the minimum effective dose used to induce the second pregnancy (5-7.5mg/day) was identical to 1/3-1/2 of the first one. The course of the second pregnancy of each case was also uneventful and the babies were all normal and mature. The magnitude of the rise in the prolactin level during the second pregnancy was smaller than that observed during the first pregnancy. The present longitudinal study throughout two consecutive pregnancies in three cases indicates that resolution of prolactinoma was resulted in some extent after withdrawal of stimulative factors associated with pregnancy. Hence, hyperprolactinemic infertile cases with intrasellar microadenoma can be subjected to bromocriptine therapies inducing consecutive pregnancies under intensive follow-up.

Adenoma↗
PubMedDate not supplied

The role of the adrenal medulla in the antihypertensive action of bromocriptine in neurogenic hypertensive dogs.

The effects of bromocriptine, a dopaminergic agent, on blood pressure were compared in normal and adrenal demedullated acute neurogenic hypertensive anesthetized dogs. The antihypertensive effect of bromocriptine (0.3 mg/kg IV) observed in intact dogs was not found in the absence of adrenal medulla. Since, in previous studies, it was found that this antihypertensive effect of bromocriptine was due to a dopaminergic mechanism the present results suggest the existence in adrenal glands of inhibitory dopaminergic receptors involved in the release of catecholamines.

Adrenal Medulla↗
PubMed1983

Changes in the sensitivity to apomorphine of dopamine receptors modulating dopamine and acetylcholine release after chronic treatment with bromocriptine or haloperidol.

The release of dopamine (DA) and of acetylcholine (ACh) was monitored from rabbit striatal slices labeled with [3H]DA and [14C]choline. Chronic treatment with haloperidol (1 mg/kg b. wt. for 28 days, sacrifice 96 hr after last injection) increased the potency of in vitro apomorphine in inhibiting the release of DA and ACh evoked by electrical stimulation when compared to vehicle-treated rabbits. Potentiation of apomorphine effects was greater on DA than on ACh release. The effects of in vitro haloperidol on DA and ACh release and in antagonizing the inhibitory effects of apomorphine were not modified by chronic treatment with haloperidol. Bromocriptine (1.5 mg/kg b.wt. for 7 days, sacrifice 72 hr after last injection) did not affect the evoked release of DA and of ACh, or the sensitivity to apomorphine. However, 15 mg/kg b.wt. of bromocriptine for 7 days and sacrifice 72 hr after last injection, produced a 60 to 70% reduction in the evoked release of DA and ACh, and markedly antagonized the inhibition of DA and ACh release produced by apomorphine. These results indicate that the DA receptors which modulate the release of DA and of ACh play an important physiological role inasmuch as they develop adaptational changes after prolonged receptor activation or inhibition by DA agonists and antagonists, respectively. These adaptational changes affect the potency of DA agonists on release modulatory receptors without modifying that of DA antagonists. The possibility that bromocriptine has a residual agonistic effect on striatal DA receptors 3 days after the last injection cannot be ruled out.

Acetylcholine↗
PubMed1982

Rapid resolution of visual field defects and reduction in macroprolactinoma size with bromocriptine therapy. A case report.

Therapy for large prolactinomas depends very much on the treatment modalities available at a particular institution. Surgery is often unsuccessful in restoring endocrine function to normal. Previous reports have demonstrated evidence of tumour regression after 3 or more months' therapy with bromocriptine (Parlodel; Sandoz). More recently, objective evidence of rapid reduction in the size of large prolactin-secreting pituitary tumours, in patients who have had no prior therapy, has been reported. We describe a patient presenting with a chiasmal syndrome and amenorrhoea due to a pituitary macro-adenoma with suprasellar extension i whom rapid tumour regrowth to its pre-operative size occurred 3 months after surgery and irradiation. Administration of bromocriptine (up to 7.5 mg/d) resulted in complete resolution of the visual field defects, radiographic evidence of tumour regression and normoprolactinaemia within 12 days of commencing bromocriptine. Further significant tumour size reduction and improved anterior pituitary function were found after another 5 weeks of therapy.

Adenoma, Chromophobe↗
PubMed1978

Bromocriptine. Clinical experience in the induction of pregnancy in amenorrhea-galactorrhea syndrome.

This study included a group of 50 women with amenorrhea-galactorrhea who were treated with bromocriptine (2-bromo-alpha-ergocryptine). Forty-two of these patients ovulated, and 36 conceived within 8 months of treatment. The pregnancies of 30 women reached a duration of 20 weeks or longer following ovulation induced by bromocriptine. Except in 1 case which ended in 10-week spontaneous abortion, the pregnancies of 26 patients terminated in 24 single, one twin, and one triplet births. All of the 29 newborns were healthy, and no congenital malformations were detected. The main side effects during treatment were transient constipation and nausea. Following delivery, return to pretreatment status was noted in all patients, which supports the fact that bromocriptine is not a curative agent.

Adult↗
PubMed1980

Superiority of bromocriptine over pyridoxine in the treatment of patients with acromegaly or galactorrhea.

Sixteen patients, eight with acromegaly and eight with galactorrhea, were treated with pyridoxine (600 mg/day) for a three-month period. The clinical and biochemical changes induced by the drug were compared with those induced by bromocriptine (2.5 to 50 mg/day) administered for the same length of time to the same patients. Pyridoxine induced lowering of growth hormone and prolactin levels in two acromegalic patients. In only one patient with galactorrhea after irradiation of the hypophysis for active acromegaly did pyridoxine treatment stop and galactorrhea and induce renewal of menstrual bleeding without significantly changing the basal prolactin levels. In another patient with a chromophobe adenoma of the hypophysis, it reduced the excessively elevated prolactin levels. On bromocriptine therapy, all the patients reported signifcant clinical improvement paralleled by significant drops in plasma growth hormone and prolactin. It appears that at the dosages administered bromocriptine is preferable to pyridoxine in the treatment of patients with acromegaly or galactorrhea.

Acromegaly↗