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PubMed1995

Effect of adding the D-1 agonist CY 208-243 to chronic bromocriptine treatment of MPTP-monkeys: regional changes of brain dopamine receptors.

1. Eleven monkeys were administered N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP): eight were treated with bromocriptine for one week and then CY 208-243 (four monkeys) or saline (four monkeys) was added to the bromocriptine treatment. 2. Addition of CY 208-243 increased the therapeutic response observed with the ergot alone without inducing dyskinesia. 3. Following MPTP, [3H]-SCH 23390 specific binding to D-1 receptors as well as [3H]-spiperone and [3H]-N-n-propylnorapomorphine specific binding to D-2 receptors increased in posterior striatum compared to control animals, whereas [3H]-SKF 38393 binding to D-1 receptors tended to decrease. 4. Dopamine receptor density was unchanged in anterior striatum of untreated MPTP-monkeys. 5. In the posterior striatum, both dopaminergic treatments decreased towards control values [3H]-SCH 23390, [3H]-spiperone and [3H]-N-n-propylnorapomorphine binding whereas they did not significantly change [3H]-SKF 38393 specific binding. [3H]-SKF 38393 specific binding increased in anterior striatum of bromocriptine-treated MPTP-monkeys, compared to untreated MPTP-animals, and this increase was abolished in animals treated with bromocriptine+CY 208-243. 6. The present study shows that in MPTP-monkeys, treated or not with DA agonists, the D1 and D2 receptor changes are concentrated in the posterior striatum and that denervation appears to cause a shift from the high to the low affinity agonist state of D1 receptors but not for the D2 subtype.

Animals↗
PubMed1985

Effect of bromocriptine on serum PTH, calcium and phosphate levels in azotemic rats.

The dopamine agonist, bromocriptine, was studied with respect to its effects on PTH secretion and calcium homeostasis in Sprague-Dawley rats made azotemic by either total or subtotal nephrectomy. The oral or intraperitoneal administration of 0.25 mg of bromocriptine resulted in a significant increase in the serum calcium concentration when compared to animals given placebo. Bromocriptine produced no significant change in the BUN or the serum concentrations of creatinine, inorganic phosphate or PTH. The mechanism of the hypercalcemic effect of bromocriptine in azotemic rats is unknown. The hypercalcemia may, however, be due to stimulation of PTH secretion, since PTH levels in the serum were inappropriately high for the corresponding levels of calcium.

Animals↗
PubMed1993

Bromocriptine, a dopamine D2 receptor agonist, inhibits adenylyl cyclase activity in rat olfactory epithelium.

The presence of large numbers of dopaminergic neurons in the olfactory bulb suggests that dopamine plays an important role in olfaction. Dopamine D2 receptors are produced in olfactory sensory neurons [Shipley et al. (1991) Chem. Senses 16, 5] and found in relatively high concentrations in their terminals in the nerve and glomerular layers of the olfactory bulb [Nickell et al. (1991) NeuroReport 2, 9-12]. In other systems D2 receptors are linked to adenylyl cyclase by an inhibitory G-protein, and activation of the receptors results in inhibition of the enzyme. We examined rat olfactory mucous membrane to determine whether the D2 receptors were linked functionally to adenylyl cyclase as they are in other tissues. Adenylyl cyclase is found in both the olfactory cilia of the sensory epithelium and olfactory nerve terminals in the bulb. Bromocriptine, a D2 receptor agonist, was added to olfactory epithelium membrane preparations from normal and unilaterally bulbectomized adult rats and the preparations were assayed for forskolin-stimulated adenylyl cyclase activity. In unoperated animals bromocriptine significantly inhibited adenylyl cyclase activity, and the inhibition was abolished following pertussis toxin treatment. In mucosa from unilaterally bulbectomized animals we saw significantly lower adenylyl cyclase activity on the operated side and a further decrease in response to bromocriptine. The data indicate that bromocriptine decreases adenylyl cyclase activity in olfactory tissue, specifically in the sensory neurons, and the reaction is dependent on a pertussis toxin-sensitive G-protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclase Inhibitors↗
PubMed2005

Evaluation of a novel vaginal bromocriptine mesylate formulation: a pilot study.

Because of the frequent side effects found with oral bromocriptine, we created two formulas of vaginal bromocriptine suppositories to compare with vaginal application of bromocriptine tablets. The formula containing bromocriptine and a releasing agent (Pluronic F127) showed an increased dissolution rate, 39-fold greater than that of the pure drug alone, and subsequently was effective in lowering serum prolactin.

Bromocriptine↗
PubMed2005

Differential pulse voltammetric determination of the dopaminergic agonist bromocriptine at glassy carbon electrode.

The electrochemical oxidation of bromocriptine at glassy carbon electrode has been carried out in Britton-Robinson (B-R) buffer solutions in the pH range 2.0-11.0 employing cyclic, linear sweep and differential pulse voltammetry (DPV). Bromocriptine showed one well-defined oxidation peak accompanied by a smaller one. The oxidation process was found irreversible. For analytical purposes, the well-resolved diffusion controlled voltammetric peak at pH 5 was critically investigated. The linear relationship between peak current height and bromocriptine concentration allowed the differential pulse voltammetric determination of the drug over a wide concentration range, from 0.04 to 5.00 microg ml(-1) with a detection limit of 0.01 microg ml(-1). A relative standard deviation of 1.44% at 0.1 microg ml(-1) level was obtained. The proposed DPV method was successfully applied for the individual tablet assay to verify the uniformity content of bromocriptine in commercial tablets.

Bromocriptine↗
PubMed1998

Neuropharmacologic treatment of hemineglect: a case report comparing bromocriptine and methylphenidate.

Individuals who have hemineglect fail to attend to stimuli presented on the side of the body contralateral to a brain lesion. Although in animal studies the severity of neglect correlates with the degree of dopamine depletion, in hemineglect patients dopamine-enhancing medications have produced inconsistent results. We present a case of hemineglect following a right cerebrovascular accident in a 68-year-old man treated consecutively with methylphenidate and bromocriptine. Tests sensitive to neglect were administered during treatment with methylphenidate, then after all medications had been discontinued, then when the patient was taking low and moderate doses of bromocriptine, and again after all medications had been discontinued for 4 and 26 days. Methylphenidate was superior to no drug treatment. Bromocriptine produced more improvement in neglect than methylphenidate. Although the patient showed an exacerbation of his neglect after withdrawal from methylphenidate, performance gains persisted after withdrawal from bromocriptine. Treatment effects appear related to medication choice, timing of drug treatment, and the adaptability of dopaminergic receptor systems.

Brain Damage, Chronic↗
PubMed1997

Neuroprotective effects of the dopamine agonists pramipexole and bromocriptine in 3-acetylpyridine-treated rats.

The neuroprotective effects of pramipexole, a dopamine agonist, were investigated in 3-acetylpyridine (3-AP)-treated Wistar rats. Bromocriptine was used as a reference compound to compare the results obtained with pramipexole. A significant reduction (P < 0.01) in cerebellar cGMP and ATP was observed 96 h after treatment with 3-AP (500 micromol/kg, i.p.). Both pramipexole and bromocriptine significantly attenuated 3-AP-induced reduction in cerebellar cGMP and ATP. Consistent with the neurochemical effect, both pramipexole and bromocriptine prevented 3-AP-induced loss of motor coordination. 3-Acetylpyridine produced a significant (P < 0.01) loss of neurons in the inferior olivary nucleus. Treatment with pramipexole and bromocriptine partially, but significantly (P < 0.01), prevented the loss of inferior olivary neurons. There was no reduction in the temperature of the animals, indicating that hypothermia was not responsible for neuroprotection.

Adenosine Triphosphate↗
PubMed1978

Normalization of visual fields following bromocriptine treatment in hyperprolactinemic patients with visual field constriction.

Two patients with galactorrhea-amenorrhea and bilateral visual field defects were studied. Routine radiologic examination of each patient revealed a normal sella turcica and no demineralization of the posterior clinoid process. Serum prolactin levels were elevated (patient V. G., 80 ng/ml; patient S. R., 204 ng/ml). Within 2 months of bromocriptine therapy, the serum prolactin levels were normal (patient V. G., 12.21 ng/ml; patient S. R., 8.25 ng/ml) and the bilateral visual field defects were corrected. Bromocriptine has been shown to control prolactin secretion in patients with prolactin-secreting pituitary tumors. Normalization of restricted visual fields following bromocriptine therapy indicates the possibility of an anatomical regression of pituitary hyperplasia or an underlying prolactin-producing microadenoma. It is speculated that the modality of functional galactorrhea reflects hyperplasia of the lactotrophs preceding a nodular and ultimately an adenomatous change. The continuous and prolonged administration of bromocriptine may prevent such a progressive sequence. Further experience is required to validate this possibility.

Adult↗
PubMed1980

Estrogenic response in women with amenorrhea during treatment with human menopausal gonadotropin with and without the simultaneous administration of bromocriptine.

In an attempt to determine whether prolactin influences estrogen biosynthesis in the ovary, the estrogenic responses of women with amenorrhea under treatment with human menopausal gonadotropin (hMG), with and without the simultaneous administration of the prolactin inhibitor bromocriptine, were investigated in a total of 20 treatment cycles. In five of the six women studied, the addition of bromocriptine produced a urinary excretion of estrogenic compounds 79% higher than that produced by treatment with hMG alone. In one woman with a slightly increased serum prolactin level, the addition of bromocriptine necessitated halving the total hMG dosage. One woman with low endogenous levels of follicle-stimulating hormone (FSH) and a limited response to gonadotropin-releasing hormone showed no increased estrogen excretion after bromocriptine administration over that produced by hMG alone. These results suggest that (1) both elevated and normal serum prolactin levels can have a direct inhibitory effect on the ovary and (2) FSH may be necessary for the formation of prolactin receptors in the ovary.

Adult↗
PubMed1980

A rationale for the use of bromocriptine in patients with amenorrhea and normoprolactinemia.

The return of menses in amenorrheic normoprolactinemic women after treatment with bromocriptine is well documented. To determine whether an increased pituitary prolactin-secreting capacity may be the underlying mechanism, 14 women with amenorrhea were studied. None complained of galactorrhea, but in all 14 it was possible to express a few drops of milk from the nipple. All women were normoprolactinemic and had normal sellar tomography. A standard thyrotropin-releasing hormone (TRH) test was performed and bromocriptine (2.5 mg twice daily) was administered. Within 8 weeks, 9 of 14 patients had return of menses. The second group of five patients did not respond to bromocriptine. The mean prolactin response to TRH was significantly greater in those women who experienced return of menses, although there was individual overlap between both groups. This finding suggests that enhanced prolactin secretory capacity may account for amenorrhea is some apparently normoprolactinemic patients. The TRH test may serve to identify those patients who may benefit from bromocriptine.

Adult↗
PubMed1985

The efficacy of bromocriptine in patients with ovulatory dysfunction and normoprolactinemic galactorrhea.

The response to bromocriptine therapy of 12 infertile women with ovulatory dysfunction and euprolactinemic galactorrhea was studied. Four of the subjects had anovulation, four had oligo-ovulation, and four had delayed ovulation. Serum PRL levels in all 12 subjects were less than 20 ng/ml. Normal ovulation occurred at least once in all of the patients on bromocriptine therapy and in 38 of 41 (92%) of the cycles. Seven patients (58%) conceived promptly with bromocriptine therapy, and all subjects had cessation of galactorrhea within 1 month of the onset of therapy. The seven pregnancies included five normal term vaginal deliveries, one premature vaginal delivery, and one tubal pregnancy. The results of this study should be considered preliminary but suggest that the presence of euprolactinemic galactorrhea in patients with ovulatory dysfunction may still represent a covert disorder of PRL physiologic factors. The prompt correction of these ovulation disturbances gives supporting evidence for this hypothesis and suggests that a short trial of bromocriptine therapy may be warranted after minimal blood sampling. The differential outcome between our group of patients produces further evidence that variable mechanisms may be operative.

Adult↗
PubMed1994

Long-acting repeatable bromocriptine in the treatment of patients with microprolactinoma intolerant or resistant to oral dopaminergics.

OBJECTIVE: To study the efficacy of long-acting repeatable bromocriptine in suppressing abnormal PRL secretion in microprolactinoma patients. To assess the incidence and nature of side effects induced by the product. DESIGN: Longitudinal, open label, noncontrolled. SETTING: Human hyperprolactinemic volunteers in an academic clinical research environment. PATIENTS: Ten patients with radiologically proven microademonas resistant or intolerant to oral bromocriptine were included. INTERVENTIONS: The patients were treated with 50 to 150 mg of long-acting bromocriptine monthly during 6 months. MAIN OUTCOME MEASURE: The serum PRL concentrations and the side-effects were assessed before and after each new injection. RESULTS: Serum PRL levels decreased during the first cycle to normal values in four patients. At the end of the study the PRL levels were normalized in five cases and were only slightly increased in three. One patient was resistant to the treatment. Two among four infertile women became pregnant. In nine patients the accompanying symptoms disappeared after the 2nd month. Adverse events were mild or moderate and circumscribed to the 1st month of treatment. CONCLUSION: The long-acting bromocriptine is both effective and well tolerated and is a good alternative to the oral approach in the management of microprolactinoma patients.

Administration, Oral↗
PubMed1987

Prolactin secretion and menstrual function after long-term bromocriptine treatment.

Long-term bromocriptine treatment was discontinued in 75 hyperprolactinemic women. Bromocriptine had been given for up to 65 months (median, 24 months). Treatment was reinstituted in 42 women (56%) after 1 to 3 months, mainly because of increasing prolactin levels. Thirty-three women (44%) were followed up for 6 months or more without treatment. Menstrual bleeding occurred in 19 of the 33 women (58%) after 6 months without treatment. The mean prolactin concentration in this group had decreased more than 60% compared with pretherapy concentrations. In 18 of the 42 women who had bromocriptine therapy again, treatment was discontinued a second time. Six of these patients have regular menstrual bleeding. Long-term bromocriptine treatment seems to induce long-standing normalization of prolactin secretion in patients with hyperprolactinemia.

Adolescent↗
PubMed2004

[Reversible postpartum cerebral angiopathy associated with bromocriptine therapy].

BACKGROUND: Postpartum is known to be an important risk factor for stroke. Bromocriptine may induce cerebral angiopathy. CASE DESCRIPTION: We report the case of a 26-year-old postpartum woman who presented with headaches, seizures, hypertension and acute renal failure eight days after the beginning of a treatment with bromocriptine prescribed for lactation suppression. Brain MRI and MR angiogram excluded cortical vein thrombosis and revealed multiple abnormal areas of increased signal in the cortex with segmental arterial narrowings of intracranial vasculitis. The patient completely recovered within one week after drug withdrawal. Biological and radiological abnormalities were also reversible. Following the chronology bromocriptine was most likely responsible for this adverse cerebral and systemic event. CONCLUSION: Clinicians should be aware of bromocripine-related postpartum cerebral angiopathy, a rarely described but serious complication of bromocriptine used to prevent postpartum breast engorgement.

Adult↗
PubMed1976

Bromocriptine and levodopa (with or without carbidopa) in parkinsonism.

Bromocriptine, a dopamine receptor agonist, was administered to 20 patients with idiopathic parkinsonism taking levodopa (L-dopa) or "Sinemet" (levodopa combined with carbidopa in a 10/1 ratio) at optimum doses. In a double-blind randomised cross-over study lasting 6 months, the addition of bromocriptine (mean daily dose 79 mg) led to a significant (P less than 0.01) 74% reduction in the dose of sinemet and levodopa. "Total disability score" showed a significant (P less than 0.01) improvement at both low and high doses of bromocriptine. Tremor improved 50% (P less than 0.01), with significant improvements in gait, posture, writing, balance, rigidity, finger dexterity, and drooling. Adverse reactions were similar to those observed with sinemet and levodopa. Although both the cause and the cure of idiopathic parkinsonism remain elusive, bromocriptine appears to represent a therapeutic advance.

Aged↗
PubMed1979

Bromocriptine associated with a peripheral dopamine blocking agent in treatment of Parkinson's disease.

A peripheral dopaminergic blocking agent, domperidone (60 mg daily), or placebo was given, double-blind, to 17 parkinsonian patients who also received increasing doses of bromocriptine. Combined treatment with domperidone reduced total disability by 76% in 8 patients receiving a mean dose of 148 mg of bromocriptine daily. There was no vomiting and involuntary movements and psychic disturbances were similar to those in patients on levodopa and a peripheral decarboxylase inhibitor. In 9 patients taking placebo instead of domperidone, the average daily dose of bromocriptine could not be raised beyond 92 mg. The mean total disability score in this group was reduced by only 48%. Thus, peripheral blockade of dopamine receptors is a promising means of limiting the adverse side-effects of the treatment of parkinsonism with central dopaminergic receptor stimulating agents such as bromocriptine.

Adult↗
PubMed1985

Visual function in prolactinoma patients treated with bromocriptine.

Ten patients with prolactin-secreting pituitary adenomas (prolactinoma) and visual dysfunction were treated primarily with bromocriptine. Nine patients had improvement of visual field or acuity associated with computed tomography (CT) evidence of a decrease in tumor size and reduction of serum prolactin level (SPL). Visual improvement usually began within days of commencing bromocriptine therapy. One patient with initial improvement had a worsening of visual fields at 11 months despite a normal SPL and a stable CT appearance of tumor size. This patient and the single patient without visual improvement underwent trans-sphenoidal hypophysectomy (TSH), but neither patient had postoperative visual improvement. Two other patients underwent TSH for nonvisual reasons. The remaining six patients have maintained excellent visual function at last follow-up (average of 18 months on bromocriptine therapy). This study shows that bromocriptine is an effective short- and long-term therapy for most patients with visual dysfunction due to prolactinoma.

Adult↗
PubMed1985

Bromocriptine and the hypothalamic hypophyseal function in patients with chronic renal failure on chronic hemodialysis.

Ten patients with chronic renal failure on chronic hemodialysis had the following tests to evaluate the integrity of the hypothalamic hypophyseal axis: (A) glucose tolerance test, (B) thyrotropin releasing hormone stimulation test, (C) clonidine stimulation test, (D) insulin induced hypoglycemia, and (E) LH/RH stimulation test. The majority of those tests were abnormal and prolactin values were found to be moderately elevated in all the patients. Bromocriptine (1.25 mg twice a day) was given to all the patients for 1 month and then, while on bromocriptine, the tests were repeated. Although there is a decrement in the concentration of serum prolactin level, none of the hypothalamic hypophyseal abnormalities were corrected. However, five of the ten patients reported an improvement of their impotence with bromocriptine. The patients who responded had high levels of FSH and LH with levels of testosterone above 1 mg/mL. The nonresponders had low FSH and LH levels and very low testosterone levels. Therefore, bromocriptine, although possibly beneficial in some dialysis patients, is not a drug that can normalize abnormal functioning of hormones in the dialysis population.

Adult↗