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PubMed1989

Bromocriptine inhibition of anesthesia-induced hyperprolactinemia: effect on serum and follicular fluid hormones, oocyte fertilization, and embryo cleavage rates during in vitro fertilization.

Thirty-two patients undergoing in vitro fertilization (IVF) were given bromocriptine either 1 or 12 hours before anesthesia or received no drug to determine what effect suppression of transient, anesthesia-induced hyperprolactinemia would have on peripheral and follicular fluid hormones, fertilization and cleavage rates, and pregnancy. Thirty minutes after anesthesia, there was a 120-ng/mL rise in serum prolactin (PRL) in control patients versus an insignificant change in women given bromocriptine. Levels of PRL in follicular fluid were significantly less, and estradiol (E2) levels were higher (P less than 0.05) in all bromocriptine-treated patients compared with controls, whereas follicular fluid levels of progesterone (P), inhibin activity, and midluteal serum P were unaffected. Although fertilization and pregnancy rates were similar, a greater proportion of fertilized oocytes from bromocriptine-treated patients advanced to cleaving embryos compared with controls (95% versus 63%, respectively; P less than 0.001). We conclude that bromocriptine, given before anesthesia, can suppress transient, anesthesia-induced hyperprolactinemia and dramatically alter follicular fluid concentrations of PRL and E2. Although these changes in hormonal milieu affected neither oocyte fertilization nor pregnancy rate in our IVF patients, they seemed to have a positive influence on embryonic development after IVF.

Adult↗
PubMed1978

Bromocriptine and prostatic carcinoma: plasma kinetics, production and tissue uptake of 3H-testosterone in vivo.

The influence of the anti-prolactin bromocriptine on plasma kinetics, production rate and tissue uptake of testosterone was investigated in 15 patients with newly diagnosed stages C and D prostatic carcinoma. Bromocriptine was given for 5 days in a daily dose of 15 mg. orally. The studies were performed with the single injection technique using the 2-compartment model. Plasma testosterone, serum prolactin, and luteinizing and follicle-stimulating hormones were determined initially. Blood samples were drawn up to 5 hours after the injection of 3H-testosterone. For tissue studies a transrectal needle biopsy was done 3 hours post-injection. Bromocriptine suppressed prolactin and the endogenous testosterone level. Furthermore, it favored the elimination of 3H-testosterone, lowered the production rate of testosterone and hampered the in vivo uptake of the 3H-label into prostatic carcinoma tissue. Finally, the grading of the tumor lesions affected only the pre-bromocriptine uptake of radioactive androgens and not the uptake in response to bromocriptine. The potential clinical impliications of these observations are discussed.

Aged↗
PubMed1997

Effects of L-dopa and bromocriptine on haloperidol-induced motor deficits in mice.

L-3,4-Dihydroxyphenylalanine (L-DOPA), the precursor of dopamine, and bromocriptine, a dopamine D2 receptor agonist, were investigated in haloperidol-induced motor impairments in mice using both catalepsy and pole tests. In catalepsy test, subcutaneous treatment with haloperidol (0.125, 0.25 and 0.5 mg/kg) caused a cataleptic effect in mice in a dose-dependent manner. This cataleptic effect was evident upto 7 hr after haloperidol treatment. In pole test, haloperidol (0.125, 0.25 and 0.5 mg/kg) produced the prolongation of Tturn and TLA as a marker of bradykinesia in mice and the prolongation lasted at least 7 hr after haloperidol treatment. Intraperitoneal co-pretreatment with L-DOPA (400 mg/kg) + carbidopa (10 mg/kg) in mice decreased the catalepsy induced by haloperidol at a dose of 0.125 mg/kg, while co-pretreatment with L-DOPA (200 and 400 mg/kg) + carbidopa (10 mg/kg) dose-dependently decreased the haloperidol (0.125 mg/kg)-induced bradykinesia. The effect of LDOPA + carbidopa in pole test was more pronounced than that in catalepsy test. Intraperitoneal pretreatment with bromocriptine (2 and 4 mg/kg) in mice reduced the catalepsy and bradykinesia produced by haloperidol at a dose of 0.125 mg/kg. The effect of bromocriptine in pole test was relatively similar to that in catalepsy test. Also, co-pretreatment with LDOPA (400 mg/kg) + carbidopa (10 mg/kg) and pretreatment with bromocriptine (2 and 4 mg/kg) significantly decreased the catalepsy induced by haloperidol at a higher dose of 0.5 mg/kg. These results indicate that co-administration with L-DOPA + carbidopa and single treatment with bromocriptine can decrease haloperidol-induced catalepsy and bradykinesia in mice. Furthermore, our study suggests that pole test as well as catalepsy test is of value in the screening of drugs against neuroleptic-induced motor deficits.

Animals↗
PubMed1979

Reduction of pituitary-tumour size in patients with prolactinomas and acromegaly treated with bromocriptine with or without radiotherapy.

69 patients with prolactin-secreting or growth-hormone-secreting pituitary tumours were treated with bromocriptine with or without pituitary irradiation and followed up for 6 months to 6 1/2 years. Of 26 patients with prolactinomas, 11 had external pituitary irradiation in addition to bromocriptine. There was evidence of shrinkage of the pituitary tumour (either a reduction in fossa size or loss of visual-field defects) in 6 of these patients (23%), 3 of whom had been treated with bromocriptine alone. Of 43 acromegalic patients, 30 received external pituitary irradiation. 8 (19%) showed evidence of shrinkage of the pituitary tumour, including 2 who had received no radiotherapy. 1 patient treated with bromocriptine alone showed striking reduction in the size of his suprasellar extension, as assessed by serial computed-tomography scans over 11 months. At the same time his visual-field defects resolved and his deficient corticotrophin and thyrotrophin reserves returned to normal. Bromocriptine can reduce the size of both prolactin-secreting and growth-hormone-secreting pituitary tumours, and this is of potential importance in their management.

Acromegaly↗
PubMed2002

Prior experience with bromocriptine in the home cage attenuates locomotor sensitization in rats.

The dopamine D(2) agonist bromocriptine has a long lasting, biphasic effect on locomotion, causing decreased activity during the first 60-90 min after the injection, followed by increased activity that peaks 90-180 min after the injection. In Experiment 1, repeated injections of 5.0 mg/kg bromocriptine produced rapid development of locomotor sensitization when rats were placed in activity chambers for 90 min immediately following each injection. Once sensitization had occurred, expression of sensitization was enhanced when the rats were tested for 90 min beginning 90 min after the injection. In contrast, when rats were placed in the activity chambers for 90 min after spending the first 90 min following each injection of bromocriptine in their home cage, the onset of locomotor sensitization was delayed and expression of sensitization was reduced. In Experiment 2, this inhibition of sensitization did not occur when rats spent the first 90 min following each injection of bromocriptine in a cage that was identical to their home cage, but was not their home cage. Thus, spending the first 90 min after the injection of bromocriptine in the home cage somehow inhibits the development of locomotor sensitization during the subsequent 90 min of each session. These data are consistent with other data indicating that repeated injections of drugs in the home cage often fail to produce the locomotor sensitization that is observed when these injections occur in novel cages.

Animals↗
PubMed2000

Bromocriptine restores angiotensin II response in pituitary hyperplasia.

In estrogen-induced pituitary hyperplasia AII-evoked prolactin release is decreased and the octapeptide does not generate a spike elevation in [Ca(2+)](i) in vitro. We studied whether or not bromocriptine could restore AII response in diethylstilbestrol treated rats. Co-administration of bromocriptine resulted in involution of pituitary size and lowering of serum prolactin. In vitro, prolactin release per cell was reduced in the hyperplastic group, and levels were not significantly increased by in vivo bromocriptine treatment. Immunocytochemical analysis revealed that hyperplastic pituitaries contained fewer prolactin granules than control pituitaries, and that bromocriptine, did not increase prolactin storage. Nevertheless, in this group, prolactin response to AII increased, and AII evoked a consistent spike in [Ca(2+)](i), albeit lower than in the control group. Such spike was abolished by thapsigargin, and not by removal of extracellular calcium or by K(+), indicating that it was mainly dependent on intracellular calcium stores, as in normal cells. We conclude that bromocriptine treatment partially restores AII response in the hyperplastic pituitary.

Angiotensin II↗
PubMed1991

Surgical outcome and pathological effects of bromocriptine preoperative treatment in prolactinomas.

The case histories of 40 patients with prolactinomas were retrospectively reviewed. Twenty patients treated preoperatively with bromocriptine were compared to 20 untreated patients. The two groups were comparable according to tumor size and sex. All the patients had an immuno-cytochemically confirmed prolactin adenoma. They were operated on by a transsphenoidal approach. Intraoperative findings were studied. The surgical cure rates (serum PRL level less than 30 micrograms/l) of the bromocriptine-treated group were higher than those of the control group, both in microprolactinomas (87.5% vs 50%) and macroprolactinomas (33% vs 17%). This improvement of surgical success rate may not be due solely to bromocriptine. Surgical cure also depends on preoperative serum PRL levels (less than 500 micrograms/l) and tumoral size (less than grade II0). Tumoral tissue remained in all cases. No increase in fibrosis was observed. By inducing tumoral shrinkage, bromocriptine makes surgical removal of macroprolactinomas easier and safer. This tumoral shrinkage could be explained not only by reduction of cell size, but also by decrease in intratumoral hemorrhage. Preoperative bromocriptine treatment does not adversely affect surgical outcome. Moreover, it may be useful in cases of macroprolactinomas with suprasellar extension.

Adult↗
PubMed2001

Neuroendocrine effects of d-fenfluramine and bromocriptine following repeated smoked cocaine in humans.

To study the consequences of repeated smoked cocaine use on central serotonergic and dopaminergic function, the effects of d-fenfluramine (d-FEN) and bromocriptine on plasma hormones were determined at three time-points following repeated cocaine self-administration under carefully controlled conditions. In a 20-day inpatient study, male cocaine abusers (d-FEN: n=10; bromocriptine: n=8) self-administered smoked cocaine (12-50 mg) for 3 days followed by 2 weeks of abstinence. The acute effects of d-FEN (0 or 30 mg po) or bromocriptine (0 or 1.25 mg po) on plasma neuroendocrine levels were determined 1-2, 7-8, and 13-14 days after the last cocaine dose. Blood was drawn before and then every 30-60 min for 4 h after capsule administration. The effects of d-FEN and bromocriptine were also determined in healthy, outpatient controls; d-FEN was removed from medical use in the US midway through the study due to complications associated with chronic administration, so all of the control participants were tested in Italy. Cocaine users had a blunted prolactin and cortisol response to d-FEN that lasted for at least 2 weeks of cocaine abstinence, but had a normal response to bromocriptine, which suppressed prolactin by 50% of baseline. The long-lasting and selective disruptions in serotonin pathways following chronic cocaine use may provide a neurochemical basis for changes in mood commonly reported during cocaine withdrawal.

Adult↗
PubMed1990

Bromocriptine in the Rett syndrome.

Twelve typical cases of the Rett syndrome and one forme fruste were treated with bromocriptine for six months and then had a washout for two months followed by resumption of the bromocriptine treatment. During the first bromocriptine treatment there were improvements in communication and relaxation in some of the girls: a more regular sleep pattern was observed in 4 and a more varied facial expression in 8, and 4 girls began to utter a few words. The bouts of hyperpnea disappeared in 5 and grinding of the teeth in 3. There was also a reduction in stereotypic hand activities in 5 girls and signs of improved motor abilities in 3. The washout caused a general decrease in the positive effects of the previously administered bromocriptine and resumption of the treatment with this drug led to less marked improvement. Metoclopramide was tested in all the girls before the treatment, and it was noted that, while endorphins were hyporesponsive, prolactin was hyperresponsive. This test was repeated two months after the bromocriptine treatment had been performed and, while beta-lipotropin remained unchanged, beta-endorphin showed increased responsiveness.

Adolescent↗
PubMed1984

Bromocriptine treatment of digitalis-induced ventricular tachyarrhythmias: studies in a canine model.

Ventricular tachyarrhythmias associated with digitalis toxicity are believed to be due, in part, to cardiac glycoside-mediated increased central sympathetic neural activity. Because dopaminergic receptor agonists reduce sympathetic outflow, this study assessed effectiveness of the available dopaminergic agonist, bromocriptine, in slowing or terminating ouabain-induced ventricular tachycardia in anesthetized dogs. In all experiments, ouabain was administered intravenously (20 micrograms/kg body weight bolus injection, followed by 2.5 micrograms/kg per min infusion) until the onset of stable ventricular tachycardia. Of seven untreated dogs (Group 1), ouabain-induced ventricular tachyarrhythmias resulted in ventricular fibrillation in three, while in four dogs tachycardia persisted without significant change in rate until the study was terminated. Fourteen dogs (Group 2) received bromocriptine, either 30 micrograms/kg (Group 2A) or 50 micrograms/kg (Group 2B), after the onset of ventricular tachycardia. Tachycardia slowed in all 14 dogs and terminated with resumption of sinus rhythm in 8 of the 14. In all six dogs pretreated with the peripheral dopaminergic antagonist domperidone (Group 3), bromocriptine, 50 micrograms/kg, slowed ventricular tachycardia and in three of the six, tachycardia terminated. In contrast, of five dogs pretreated with haloperidol, a central and peripheral dopaminergic receptor antagonist (Group 4), bromocriptine, 50 micrograms/kg, failed to slow ventricular tachycardia in three, and two of the three developed ventricular fibrillation. In summary, the dopaminergic receptor agonist, bromocriptine, presumably acting at central dopaminergic receptor sites, consistently slowed and in most cases reversed ouabain-induced ventricular tachycardia in a canine model.

Animals↗
PubMed1999

Repeated co-administration of caffeine and bromocriptine prevents tolerance to the effects of caffeine in the turning behavior animal model.

The present study examined the effects of repeated co-administrations of caffeine and bromocriptine for 9 consecutive days on contralateral turning in unilateral nigrostriatal 6-hydroxydopamine denervated rats. In agreement with previous data, our results showed that on the first administration, both caffeine and bromocriptine injected plus saline produced a significant increase in contralateral rotational behavior as compared to saline-saline injections. However, with repeated administrations, tolerance was observed to caffeine, but not to bromocriptine. The combination of different doses of bromocriptine (0.1, 0.2, 0.4 and 0.8 mg/kg) with caffeine (40 mg/kg) significantly enhanced the effects of either drug injected with saline on rotational behavior, and no tolerance was observed with repeated treatment. The continuous co-administration of both substances was necessary to maintain elevated levels of rotational behavior, since withdrawing one or the other drug led to decreased contralateral turning. These results demonstrate that when caffeine is administered repeatedly in combination with bromocriptine, tolerance to its psychostimulant effects is not observed, suggesting that caffeine could be used as an adjunctive therapeutic agent with dopamine agonists for the treatment of Parkinson's disease.

Adrenergic Agents↗
PubMed1984

Bromocriptine in Parkinson's disease: results obtained with high and low dose therapy.

The results obtained with high and low dose bromocriptine therapy were compared in a review assessing the per cent of patients showing improvement (not taking account of the extent of improvement). It is concluded that the response rate with low dose bromocriptine is as good as that obtained with high dose therapy for both de novo and levodopa treated patients. The incidence of adverse effects is similar in the high and low dose treatment groups. More levodopa reduction results in a higher daily bromocriptine requirement. A statistical analysis of 61 bromocriptine-levodopa treated patients showed no positive correlation between bromocriptine dose and severity or duration of Parkinson's disease.

Bromocriptine↗
PubMed2003

Blunted central bromocriptine-induced tachycardia in conscious, malnourished rats.

Bromocriptine-induced tachycardia, persisting after adrenalectomy, is mediated by central dopamine D2 receptor stimulation through activation of the sympathetic outflow to the heart. The present study investigated the effects of malnutrition during pregnancy on bromocriptine-induced tachycardia in adult conscious rats. Malnourished rats were obtained by feeding dams a multideficient diet (providing 8% protein) during mating and pregnancy. Birth weight was significantly reduced in malnourished rats when compared to control rats born to dams fed standard commercially diet (23% protein) during mating and pregnancy. Baseline mean aortic pressure and heart rate in malnourished rats were comparable to those of well-nourished rats. Tachycardia (33+/-9 beats/min.), but not the hypotensive response to intravenous bromocriptine (150 microg/kg) was significantly reduced in malnourished rats, compared with control rats (70+/-10 beats/min.). In malnourished rats, pretreatment with intravenous domperidone (500 microg/kg) blocked the bromocriptine-induced hypotension, without affecting the tachycardia. Neither cardiac vagal (40+/-6 beats/min.) nor sympathetic tone (76+/-6 beats/min.) was significantly altered by multideficient diet-induced malnutrition (51+/-6 and 67+/-10 beats/min., respectively). In isolated perfused heart preparations from malnourished rats, positive inotropic response to isoproterenol (10-8 to 10-4 M) was not significantly different compared to that in control rats. In summary, malnutrition during foetal life blunted the bromocriptine-induced tachycardia, an effect that could be related to central dopamine D2 receptor desensitization rather than to impairment of autonomic regulation of the heart or cardiac beta-adrenoceptor desensitization.

Animals↗
PubMed1992

Enhancement of dopaminergic agonist bromocriptine of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats.

The effects of the dopamine agonist 2-bromo-alpha-ergocryptine methanesulfonate (bromocriptine) on the incidence, number and histology of gastric cancer induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. Rats were given 1 or 2 mg kg-1 body weight of bromocriptine subcutaneously every other day in depot form after 25 weeks of oral treatment with MNNG. Prolonged administration of bromocriptine at both dosages every other day resulted in a significant increase in the incidence and number of gastric cancers of the glandular stomach by week 52. Bromocriptine treatment did not influence the histological type of gastric cancer, but caused a significant increase in the labelling index of epithelial cells of the antrum. These findings indicate that the dopamine agonist bromocriptine promotes gastric carcinogenesis, and that this effect may be related to its effect in increasing proliferation of epithelial cells in the antral mucosa.

Adenocarcinoma↗
PubMed2000

Bromocriptine reduces cigarette smoking.

AIMS: Animal studies have shown that nicotine releases dopamine, a neurotransmitter implicated in drug reinforcement. We hypothesized that bromocriptine would decrease smoking behavior in humans. DESIGN: The study was conducted double blind and subjects' order of dose exposure was randomized. PARTICIPANTS: The smoking behavior of 20 heavy smokers was recorded for 5 hours after ingesting placebo or one of two doses of bromocriptine (2.50 mg, 3.75 mg) over three sessions (one dose per session). FINDINGS: There was a significant negative linear trend by dosage indicating shorter total puffing time with increasing bromocriptine dosages (p < 0.02). Other significant negative linear trends by increasing dosage include fewer number of puffs, fewer number of cigarettes smoked and mean latency to smoke after 3 hours (expected CMAX on the drug (all ps < 0.05). There was a negative significant linear trend showing decreased plasma nicotine (p < 0.02) and cotinine (p < 0.005) with increasing dosages of bromocriptine. Shiffman/Jarvik Withdrawal Scale (SJWS) cigarette craving subscale scores decreased significantly across increasing dosages (linear trend p < 0.02). There was a significant negative linear trend (p < 0.05) on the Profile of Mood States (POMS) Vigor and Depression subscales, with subjects reporting decreased vigor and depression with increasing bromocriptine doses. No other mood effects were observed. CONCLUSION: These results support the hypothesis that dopaminergic mechanisms mediate cigarette smoking reinforcement.

Adolescent↗
PubMed1984

Effect of a somatostatin analogue on trophic hormone levels in acromegalic patients with elevated hGH after adenomectomy and treatment with bromocriptine.

Five female acromegalic patients who had undergone surgical adenomectomy, but still had elevated hGH serum levels, were treated with bromocriptine, 5-15 mg daily, for at least 4 months without a satisfactory response. In an attempt to lower serum hGH levels, p-NH2-Phe4-D-Trp8-somatostatin was administered, 100 micrograms as an i.v. bolus, followed by infusion of 250 micrograms over a 4 hour period. The analogue decreased hGH levels by about 50% in 3 out of 5 patients, both during bromocriptine treatment and also in its absence. Of the remaining two patients, one showed a decrease in hGH levels in response to the analogue only during bromocriptine treatment and the other only without it. Saline infusion after bromocriptine administration did not induce a decrease in hGH levels in three of these patients. Somatostatin analogue caused a fall in serum insulin levels in all but one patient, who had diabetes mellitus and in whom serum insulin was undetectable. Both hGH and insulin levels showed a significant rebound after infusion of the analogue, but returned to basal levels within 24 hours. Prolactin did not change during the analogue infusion in 4 patients with normal PRL levels. However, in one patient in whom prolactin and hGH levels were elevated during bromocriptine treatment, the infusion of somatostatin analogue decreased both hormones. The analogue induced no changes in serum TSH, FSH and LH levels of any of the patients.

Acromegaly↗
PubMed1991

Bromocriptine in augmentation of antipsychotic response in chronic schizophrenia: a negative pilot report.

To further assess the usefulness of bromocriptine in treatment of schizophrenia seven inpatient chronic schizophrenics with acute exacerbation who had failed to respond to four weeks of antipsychotic therapy were treated with bromocriptine 2.5 mg daily for a treatment duration varying from one dose to four weeks while their antipsychotic dose was continued unchanged. Mean age of patients was 38.9 +/- 11.6 years and mean number of prior psychiatric hospitalizations was 12.0 +/- 7.2. Patients were rated with the Brief Psychiatric Rating Scale prior to the first bromocriptine dose, at 24 hours after dosage initiation, and at weekly intervals. One patient showed clinically significant improvement in both positive and negative schizophrenic symptoms. One patient showed slight improvement in unusual thought content, and four patients were clinically unchanged. One patient significantly worsened after the first dose. Factors possibly contributing to response and non-response are discussed. This is a report of an open study in 7 patients. It is the only report of bromocriptine treatment in patients previously shown unresponsive to antipsychotics and whose antipsychotics dose was held constant throughout the study. Addition of bromocriptine to the antipsychotic regimen remains an unproven treatment approach which may be considered only in patients refractory to or inadequately controlled with antipsychotics.

Adult↗
PubMed1982

Bromocriptine in tardive dyskinesia.

Five schizophrenics and one alcoholic with tardive dyskinesia were given bromocriptine for two 8-week periods. The first trial was made during neuroleptic treatment and the second following a 3 weeks' wash-out of neuroleptics. When neuroleptics were given bromocriptine was essentially without effects, but after the neuroleptics had been discontinued the same bromocriptine treatment caused amelioration of dyskinesia in three and aggravation in two subjects. During the second bromocriptine trial all schizophrenic patients showed deterioration of psychotic symptoms followed by a reduction of symptoms when bromocriptine was discontinued.

Aged↗