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PubMed2004

Cyclosporine and bromocriptine-induced suppressions of CYP3A1/2 and CYP2C11 are not mediated by prolactin.

The purpose of this study was to determine if the suppression of hepatic CYP3A1/2 (cytochrome P450 3A1/2) and CYP2C11 (cytochrome P450 2C11) by cyclosporine is mediated by prolactin. Male intact rats were given subcutaneous doses of either 15 mg/kg/day of cyclosporine or 1 ml/kg/day of cyclosporine vehicle concomitantly with one of the following: 500 mg/kg prolactin, 1 ml/kg prolactin vehicle, 4 mg/kg bromocriptine, or 1 ml/kg bromocriptine vehicle for 14 days. Protein expressions were measured using Western blot analysis and activities were measured using an in vitro testosterone hydroxylation assay. The administration of prolactin did not significantly alter CYP3A1/2 protein expression. Hypoprolactinemia, produced by bromocriptine, caused a significant suppression of CYP3A1/2 activity levels when bromocriptine was administered alone and in combination with cyclosporine (P<0.001, P<0.05; respectively). However, the cause of the suppression by bromocriptine was likely not the result of lowering prolactin levels. Bromocriptine administration also lowered CYP2C11 protein expression and activity, while prolactin administration had virtually no effect on CYP2C11. Chronic cyclosporine administration caused a 140% increase in prolactin area under the curve (AUC) (P<0.001). Bromocriptine caused a significant decline in endogenous prolactin secretion, however, concurrent cyclosporine administration did not recover these levels. Overall, while both cyclosporine and bromocriptine, separately, can significantly alter the fate of hepatic P450 enzymes, the suppression is likely not due to an alteration in prolactin levels.

Animals↗
PubMed2000

Cross-sensitization between the motor activating effects of bromocriptine and caffeine: role of adenosine A(2A) receptors.

The acute motor response to caffeine was studied in rats repeatedly treated with vehicle or the dopamine D(2) agonist bromocriptine either in a novel cage or in the home cage. Rats receiving bromocriptine (5 mg/kg i.p.) in a novel cage were sensitized to the motor stimulating effects of bromocriptine itself and showed cross-sensitization to the acute administration of low (10 mg/kg s.c. ) but not high (25 mg/kg s.c.) doses of caffeine, no matter if the novel cage was identical or different from the test cage. In contrast, caffeine (10 mg/kg i.p.) administered to rats which had received bromocriptine (5 mg/kg i.p.) in the home cage and which showed no sign of a sensitized response to bromocriptine, failed to show an increased locomotor and stereotyped response as compared to vehicle pretreated rats. Similarly to caffeine, the selective adenosine A(2A) antagonist SCH 58261 (3 mg/kg i.p.) showed an increased motor response in bromocriptine sensitized rats. The sensitized response to caffeine or SCH 58261 did not appear to be due to an higher basal motor activity of bromocriptine sensitized rats since acute administration of vehicle induced a similar motor response in bromocriptine and vehicle pretreated rats. Dopamine D(2) and adenosine A(2A) receptors are colocalized in striatal efferent neurons where they control in an opposite direction motor behavior. The results of the present study showed that changes in the sensitivity of D(2) receptors influenced the sensitivity of the adenosine antagonist caffeine through an action on A(2A) receptors. D(2) and A(2A) receptors, therefore, not only acutely interact in the mediation of motor behavior but long-term modification of the D(2) receptors, such as sensitization, affected the response of adenosine A(2A) receptors.

Animals↗
PubMed1996

Oral prednisolone supplement abolishes the acute adverse effects following initiation of depot bromocriptine therapy.

OBJECTIVE: Although an effective treatment for hyper-prolactinaemia, initiation of bromocriptine therapy may be associated with significant acute side-effects in some patients, particularly nausea, vomiting and postural hypotension. These may be minimized by initial treatment with i.m. depot bromocriptine (Parlodel-LAR, Sandoz, Basel, Switzerland), but adverse effects following the first injection may still be a significant problem. Following the observation that cortisol deficient patients were subject to an increased incidence of severe side-effects on initiation of bromocriptine therapy, we have evaluated whether concurrent administration of oral prednisolone to patients without cortisol deficiency might reduce adverse effects. DESIGN: Double-blind placebo-controlled trial with prednisolone (20 mg) prior to, and 16 hours after, depot injection of i.m. bromocriptine (50 or 100 mg). PATIENTS: Twenty-one consecutive patients with hyperprolactinaemia (serum prolactin > 1000 mU/l on 3 separate occasions) who were due to start depot bromocriptine and who had a normal cortisol response to insulin-induced hypoglycaemia. MEASUREMENTS: Symptoms at 0, 16 and 40 hours after injection were assessed using visual linear analogue scales and both inter and intra-group scores were compared by non-parametric tests. RESULTS: Depot bromocriptine was associated with the significant occurrence of light-headedness and lethargy in the placebo-administered group by 16 hours, and also with nausea and nasal congestion by 40 hours. These symptoms did not occur in the prednisolone-administered group. CONCLUSIONS: Concurrent oral administration of prednisolone significantly reduces the incidence of acute adverse effects following depot bromocriptine. Two 20 mg doses of prednisolone given at 12-hour intervals may be used to avoid dopamine-agonist-induced adverse effects at the initiation of treatment with depot bromocriptine, and may also be of value in the treatment of side-effects associated with other dopamine agonist drugs.

Administration, Oral↗
PubMed1994

A comparison of cabergoline and bromocriptine in the treatment of hyperprolactinemic amenorrhea. Cabergoline Comparative Study Group.

BACKGROUND: Cabergoline is a long-acting dopamine-agonist drug that suppresses prolactin secretion and restores gonadal function in women with hyperprolactinemic amenorrhea. We designed a study to compare its safety and efficacy with those of bromocriptine, which has been the standard therapy. METHODS: A total of 459 women with hyperprolactinemic amenorrhea were treated with either cabergoline (0.5 to 1.0 mg twice weekly) or bromocriptine (2.5 to 5.0 mg twice daily), administered in a double-blind fashion for 8 weeks and subsequently in an open fashion for 16 weeks, during which adjustments in the dose were made according to the response. Of the 459 women, 279 had microprolactinomas, 3 had macroprolactinomas, 1 had a craniopharyngioma, 167 had idiopathic hyperprolactinemia, and the remainder had an empty sella. Clinical and biochemical status was assessed at 2-week intervals for 8 weeks and monthly thereafter for a total of 6 months, with an additional assessment at 14 weeks. RESULTS: Stable normoprolactinemia was achieved in 186 of the 223 women treated with cabergoline (83 percent) and 138 of the 236 women treated with bromocriptine (59 percent, P < 0.001). Seventy-two percent of the women treated with cabergoline and 52 percent of those treated with bromocriptine had ovulatory cycles or became pregnant during treatment (P < 0.001). Amenorrhea persisted in 7 percent of the cabergoline-treated women and 16 percent of the bromocriptine-treated women. Adverse effects were recorded in 68 percent of the women taking cabergoline and 78 percent of those taking bromocriptine (P = 0.03); 3 percent discontinued taking cabergoline, and 12 percent stopped taking bromocriptine (P < 0.001) because of drug intolerance. Gastrointestinal symptoms were significantly less frequent, less severe, and shorter-lived in the women treated with cabergoline. CONCLUSIONS: Cabergoline is more effective and better tolerated than bromocriptine in women with hyperprolactinemic amenorrhea.

Adolescent↗
PubMed1989

The influence of levodopa in the pharmacokinetics of bromocriptine in Parkinson's disease.

The administration of bromocriptine in addition to levodopa in Parkinson's disease produces beneficial results. Several hypotheses have explained the advantage of the combined treatment by a pharmacodynamic interaction in the striatum. However, no study has considered the possibility that levodopa modifies the kinetics of bromocriptine. In the present study performed with parkinsonian patients, we measured blood levels of bromocriptine (by radioimmunoassay) at 0, 30, 60, 90, 120, 180, and 240 min after the oral administration of bromocriptine alone and together with 250 mg levodopa plus 25 mg DCI. After loading of bromocriptine alone, we found mean peak levels at 60 min (1.42 ng/ml) and at 90 min (1.82 ng/ml). These values were reduced by levodopa (0.97 ng/ml at 60 min and 0.93 ng/ml at 90 min). Although we did not observe substantial clinical differences among the groups after the drug challenge (Webster scale), this study supports our previous findings and suggests that one of the advantages of a combined treatment may result from a modification of the plasma levels of bromocriptine by levodopa. A "smoothing" of the plasma bromocriptine curve possibly avoids sudden oscillations of the drug and enables a more "stable" penetrability of the medication into the central nervous system. Therefore long-term combined treatment is advised in preference to bromocriptine alone.

Adjuvants, Pharmaceutic↗
PubMedDate not supplied

Double-blind, crossover, placebo-controlled trial of bromocriptine in patients with sleep bruxism.

This study was designed to assess the effects of bromocriptine, a dopamine D2 receptor agonist, on sleep bruxism. Seven otherwise healthy patients with severe and frequent sleep bruxism participated in this randomized, double-blind, placebo-controlled study. The study used a crossover design that included 2 weeks of active treatment or placebo with a washout period of 1 week. To further evaluate whether bromocriptine influences striatal D2 receptor binding, we used iodine-123-iodobenzamide single photon emission computed tomography (SPECT) under both placebo and bromocriptine regimens. Bromocriptine did not reduce the frequency of episodes of bruxism during sleep (mean +/- SEM, 9.0 +/- 1.0 and 9.6 +/- 1.5 bruxism episodes per hour for placebo and bromocriptine, respectively) or the amplitude of masseter muscle contractions (root mean square values, 48.2 +/- 15.5 microV and 46.9 +/- 12.7 microV for placebo and bromocriptine, respectively). SPECT also failed to reveal that either treatment had any influence on striatal D2 binding (values for total binding in counts/pixel, 1.80 [1.72-1.93] and 1.79 [1.56-1.87] for placebo and bromocriptine, respectively). This study shows that a nightly dose of bromocriptine does not exacerbate or reduce sleep bruxism motor activity.

Adult↗
PubMed1993

Control of prolactin-secreting macroadenomas with parenteral, long-acting bromocriptine in 30 patients treated for up to 3 years.

OBJECTIVE: We investigated the effect of intramuscular injections of long-acting bromocriptine in patients with macroadenomas. STUDY DESIGN AND PATIENTS: Thirty patients with PRL-secreting pituitary macroadenomas were treated with repeated 4-weekly intramuscular injections of 50 or 100 mg of a long-acting, repeatable bromocriptine formulation for six to 37 injections, amounting to a total of 473 injections. Twenty patients received parenteral bromocriptine as primary therapy, ten had persisting hyperprolactinemia after previous therapies including pituitary surgery (n = 7), oral bromocriptine (7), and pituitary irradiation (2). MEASUREMENTS: A PRL day profile was obtained and the patients' clinical status and history were documented, at intervals. Detailed clinical, laboratory, and radiological (pituitary nuclear magnetic resonance or computed tomography scan) evaluations were performed at baseline, after 1 injection and every 6th injection thereafter. RESULTS: In all patients PRL was suppressed from a mean +/- SEM pretreatment level of 32,620 +/- 8680 to 4480 +/- 1140 mU/I on the third day after the first injection. In 12 patients PRL levels normalized (< 400 mU/I) with the first to fourth injection, in three additional patients PRL levels normalized after 8-15 months. In 19 patients PRL was suppressed to less than 1000 mU/l. In three patients PRL did not decrease to less than 50% of pretreatment; in two of them on oral bromocriptine prior to this study there had been a comparable low efficacy. Of 28 patients with macroadenomas (median height 22 mm) tumour shrinkage was evident in 15 by nuclear magnetic resonance or computed tomography scan 28 days after the first injection, and in three additional patients after 6 months. There was further regression in seven cases after 12, 18 or 24 injections. Adenoma size (mean +/- SEM) decreased to 66 +/- 7% of the pretreatment value. The 40 adverse events noted in 20 of 30 patients during 24 hours after the first injection were similar to known side-effects of oral bromocriptine, nausea and postural hypotension being the most frequent. With repeated injections, on average 0.6 adverse events were noted per injection (mostly mild asthenia). There were no local adverse reactions at the injection site. CONCLUSION: We conclude that long-acting repeatable bromocriptine in patients with macroprolactinomas offers a safe and efficacious primary treatment that ensures compliance and gives long-term control. Adverse reactions are comparable to oral bromocriptine but subside with repeated injections.

Adolescent↗
PubMed1994

Treatment with octreotide and bromocriptine in patients with acromegaly: an open pharmacodynamic interaction study.

OBJECTIVE: Several studies suggest that the combination of octreotide and bromocriptine is more effective than octreotide alone in reducing GH levels in patients with acromegaly. However, these studies have evaluated either the acute effects of single doses of octreotide and bromocriptine, or the effects of long-term combination therapy, in which octreotide was given only twice a day. The aim of the study was to evaluate the effects of the combination of octreotide and bromocriptine compared to octreotide alone, using a treatment scheme of three daily injections of octreotide during a period long enough to ensure a pharmacokinetic and pharmacodynamic steady state. PATIENTS: Eleven patients with acromegaly. DESIGN AND MEASUREMENTS: Different treatment regimes were performed during three periods. During the first period there was no administration of octreotide or bromocriptine, during the second period 100 micrograms octreotide was given subcutaneously three times a day, and during the third period 100 micrograms octreotide was given subcutaneously three times a day in combination with bromocriptine, given orally 5 mg twice daily. When the patients were without any treatment a single oral dose of 5 mg bromocriptine was given at 0730 h. Individual GH levels were assessed as the mean value of 11 observations during the day, at hourly intervals from 0730 to 1530 h, and at 1730 and 1930 h, and the GH levels for the whole group were calculated as the mean of the individual mean values. Serum IGF-I and PRL were measured in fasting samples at 0730 h on the same days as GH, GH, IGF-I, and PRL were evaluated at the end of each treatment regime. RESULTS: Basal mean GH value for all 11 patients was 54.2 +/- 17.4 mU/l. During octreotide therapy mean GH value was significantly reduced compared to basal mean GH level; 19.86 +/- 6.82 mU/l (P < 0.05). The reduction of mean GH during combination therapy was also significant compared to basal, 18.70 +/- 6.72 mU/l (P < 0.05). Basal mean IGF-I value for all 11 patients was 716 +/- 96 micrograms/l. During octreotide therapy mean IGF-I value was significantly reduced compared to basal mean IGF-I level; 458 +/- 100 micrograms/l (P < 0.05). The reduction of mean IGF-I during combination therapy was also significant compared to basal, 456 +/- 93 micrograms/l (P < 0.05). There was no difference between the levels of mean IGF-I during the two treatment periods. One patient, the only patient with hyperprolactinaemia, showed an additional reduction of GH levels of > 50% during combination therapy. This was also the patient showing the most pronounced reduction of GH levels after the administration of a single dose of bromocriptine. CONCLUSION: When octreotide is administered three times a day, the additive effect of bromocriptine on GH and IGF-I suppression seems to be negligible in most patients with acromegaly.

Acromegaly↗
PubMed2004

Dopamine D2-like receptor agonist bromocriptine protects against ischemia/reperfusion injury in rat kidney.

BACKGROUND: Dopamine, via activation of D1-like and D2-like receptors, plays an important role in the regulation of renal sodium excretion. Recently, we demonstrated that dopamine D2-like receptor agonist (bromocriptine) stimulates p44/42 mitogen-activated protein kinases (MAPKs) and Na+,K(+)ATPase (NKA) activity in proximal tubular epithelial cells. Since both these parameters are compromised in ischemia/reperfusion (I/R) injury to the kidney, we investigated whether bromocriptine protects against the injury. METHODS: In this study we used unilateral rat model of renal I/R injury. The Sprague-Dawley rats were divided into vehicle and bromocriptine groups. The vehicle and bromocriptine group was treated with vehicle and bromocriptine (500 microg/kg intravenously), respectively, 15 minutes before the induction of unilateral ischemia followed by 24- or 48-hour reperfusion. At the end of 24 or 48 hours the animals were sacrificed to collect control and ischemic kidney cortices, in which necrosis, apoptosis, NKA activity, NKA alpha1 subunit expression, and p44/42 MAPK phosphorylation were measured. RESULTS: We found extensive necrosis, apoptosis, and decreased NKA activity (with no change in alpha1 subunit) in the ischemic kidney cortex compared to the nonischemic cortex from the vehicle-treated rats as early as 24 hours post-reperfusion. In contrast, I/R injury-induced necrotic, apoptotic, and decrease in NKA activity were absent in the outer cortex of bromocriptine-treated rats after 24 or 48 hours. Interestingly, we detected significantly higher phosphorylation of p44/42 MAPKs in control and ischemic kidneys of bromocriptine-treated rats compared to those of vehicle-treated rats. CONCLUSION: Therefore, bromocriptine, a D1-like receptor agonist, may protect against I/R injury to proximal tubules of the kidney, via p44/42 MAPK activation.

Animals↗
PubMed1986

Effect of bromocriptine treatment on circulating somatomedins in tall adolescents.

Somatomedin and bromocriptine levels were measured before and after 3 months of bromocriptine treatment (5 mg/day) in the sera of 16 tall adolescents with excessive adult height prediction. Somatomedins were measured by RIA for somatomedin C and IgFII and by measuring thymidine incorporation into human lectin-activated lymphocytes. Mean +/- SEM levels of bromocriptine after three months of treatment were 0.61 +/- 0.08 ng/ml. No changes in radioimmunoassayable somatomedin C were observed after bromocriptine intake respectively 1.34 +/- 0.17 U/ml before and 1.4 +/- 0.01 U/ml during treatment. On the opposite a significant decrease of thymidine activity (p less than 0.002) from 1.45 +/- 0.17 U/ml to 1.12 +/- 0.19 U/ml was observed. No changes of IgFII levels were observed in the sera of the 8 patients where they were measured. In order to test a possible direct effect of bromocriptine on peripheral tissues bromocriptine mesylate was added in somatomedin bioassays. Inhibitory effect of bromocriptine in vitro is seen at higher levels (1 microM) compared to the circulating one (1 nM). This study demonstrates that the major effect of bromocriptine which is the acceleration of bone maturation is not related to changes in somatomedin C.

Body Height↗
PubMed1991

Single dose cabergoline versus bromocriptine in inhibition of puerperal lactation: randomised, double blind, multicentre study. European Multicentre Study Group for Cabergoline in Lactation Inhibition.

OBJECTIVE: To compare the efficacy and safety of a single dose of 1 mg of cabergoline with that of bromocriptine 2.5 mg twice daily for 14 days in the inhibition of puerperal lactation. DESIGN: Prospective, randomised, double blind, parallel group, multicentre study. SETTING: University of hospital departments of obstetrics and gynaecology in different European countries. SUBJECTS: 272 puerperal women not wishing to lactate (136 randomised to each drug). INTERVENTIONS: Women randomised to cabergoline received two 0.5 mg tablets of cabergoline and one placebo tablet within 27 hours after delivery and then placebo twice daily for 14 days. Those randomised to bromocriptine received 2.5 mg of bromocriptine and two placebo tablets within 27 hours and then 2.5 mg of bromocriptine twice daily for 14 days. MAIN OUTCOME MEASURES: Success of treatment (complete or partial) according to milk secretion, breast engorgement, and breast pain; rebound symptomatology; serum prolactin concentrations; and number of adverse events. RESULTS: Complete success was achieved in 106 of 136 women randomised to cabergoline and in 94 of 136 randomised to bromocriptine and partial success in 21 and 33 women respectively. Rebound breast symptomatology occurred respectively in five and 23 women with complete success up to day 15 (p less than 0.0001). Serum prolactin concentrations dropped considerably with both drugs from day 2 to day 15; a prolactin secretion rebound effect was observed in women treated with bromocriptine. cabergoline and 36 receiving bromocriptine (p = 0.054), occurring most during the first treatment day. CONCLUSION: A single 1 mg dose of cabergoline is at least as effective as bromocriptine 2.5 mg twice daily for 14 days in preventing puerperal lactation. Because of the considerably lower rate of rebound breast activity and adverse events and the simpler administration schedule cabergoline should be the drug of choice for lactation inhibition.

Adult↗
PubMed2004

Does bromocriptine improve glycemic control of obese type-2 diabetics?

BACKGROUND: Various oral hypoglycemic agents have already been administered to type-2 diabetic patients to normalize their plasma glucose concentrations but they have not had complete and sustained success. In recent years, bromocriptine has been tried with controversial results. In present study, the effect of bromocriptine on glycemic control was evaluated in obese type-2 diabetic patients. METHODS: In a double-blind placebo-controlled clinical trial, 40 obese patients with type-2 diabetes (aged 32-70 years) were randomly allocated to the two treatment groups. The first group received bromocriptine (2.5 mg daily) for a total of 3 months. The second group received placebo. They had been uncontrolled on fixed doses of glibenclamide or its combination with metformin in the 3 months before enrolling in the study. The fasting plasma glucose (FPG) level and glycosylated hemoglobin (HbA1) were measured and body mass index (BMI) was calculated before and 1, 2 and 3 months after treatment. RESULTS: The FPG level decreased in the bromocriptine-treated group from 10.59 +/- 0.42 to 9.06 +/- 0.41 mmol/l (mean +/- SEM; p < 0.01), whereas in the placebo group it was not changed, 10.69 +/- 0.52 and 10.6 +/- 0.57 mmol/l, respectively. The HbA1 concentration was reduced in the bromocriptine-treated group from 9.9 +/- 0.3 to 9.5 +/-0.2% (p = 0.06), whereas it increased in the placebo-treated group from 10.2 +/- 0.3 to 11.3 +/- 0.6% (p < 0.05). The differences in HbA1 (1.8%, p < 0.01) and FPG (1.55 mmol/l, p < 0.05) levels between the bromocriptine and placebo groups at 3 months were significant. No changes in body weight or BMI occurred during the study in either placebo- or bromocriptine-treated group. CONCLUSION: The data further support the contention that bromocriptine improves glycemic control in obese type-2 diabetic patients, although the mechanism of action remains to be determined.

Adult↗
PubMed1992

Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients. Final report.

Final results of the 5-year multicentric collaborative study on the long-term effects of bromocriptine in the patients with Parkinson's disease are reported. This prospective study started in May 1985 in order to see whether the early combination therapy with bromocriptine and levodopa is really superior to the levodopa monotherapy with regard to the late side effects of levodopa in the treatment of parkinsonian patients. Another project of the study was to see the therapeutic efficacy of bromocriptine monotherapy without concomitant use of levodopa. For these purposes, a total of 702 patients with Parkinson's disease were enrolled into three groups: Group 1 (n = 286) with bromocriptine monotherapy, Group 2A (n = 216) with early combination of bromocriptine and levodopa, and Group 2B (n = 200) with levodopa alone. At the end of the 5-year study, 48 patients in Group 1 (16.8%) were still continuing bromocriptine monotherapy with satisfactorily good therapeutic effects. About half (49.1%) of the Group 2A patients remained on the combined therapy, and the comparable number of the Group 2B patients (46.0%) were also kept on the initial mode of therapy, while 13.5% of the latter group with levodopa monotherapy needed bromocriptine to be added in order to assure the good therapeutic effects. Moreover, significant differences were seen between group 2A and Group 2B with regard to the incidence of wearing-off phenomenon and dyskinesias. Disappearance rate of dyskinesias which were present at the time of enrollment was significantly higher in Group 2A than in Group 2B. No significant difference was noted as to the incidence of untoward symptoms and the death rate among all three therapeutic groups. These results support the view that the early combination of bromocriptine with levodopa is superior to levodopa alone in the treatment of Parkinson's disease.

Activities of Daily Living↗
PubMed1992

Nation-wide collaborative study on the long-term effects of bromocriptine in the treatment of parkinsonian patients: analysis on the maintenance and the change of the original mode of treatment.

A nation-wide collaborative study to evaluate the long-term effects of bromocriptine in patients with Parkinson's disease was completed as described in the accompanying paper. The present study analysed the same data by paying attention to a group of patients who maintained the original mode of therapy and to a group of patients who changed the mode of treatment by adding levodopa or bromocriptine to the original drug. Surprisingly, 48 among 286 patients in a group of bromocriptine monotherapy maintained the original mode of therapy. This group has particular features of a short duration of illness and a low grade of Hoehn-Yahr's scale. It is noteworthy that this group of patients did not show wearing-off phenomenon. The effects of additional bromocriptine to levodopa for a 5-year period were analysed by comparing two groups of combination therapy and levodopa alone therapy maintained for 5 years, with 106 and 92 patients, respectively. Results were essentially the same as those obtained from the accompanying paper, i.e., in general, treatment by combination with bromocriptine may be more suitable than treatment by levodopa alone. In order to find the best timing of the combination of levodopa and bromocriptine, results of 3 groups were compared, i.e. a group of patients who started with bromocriptine alone and later added with levodopa (82 patients), a group of patients who maintained the combination for 5 years (106 patients) and a group of patients who started with levodopa alone and later added bromocriptine (27 patients). The best results were obtained in the group of 5-year combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1993

Progress note on Japanese multicenter bromocriptine monotherapy.

The nationwide multicenter collaborative study for evaluating the monotherapy of Parkinson's disease with bromocriptine for a period of 5 years from 1986 was reviewed last year. The present report summarizes the follow-up in its 6th year: it includes 30 patients with Parkinson's disease who continued to receive bromocriptine monotherapy for 6 years and 66 patients who received bromocriptine-levodopa combination therapy during the same period. The mean daily dose of bromocriptine in the 6th year was about the same in the two groups (11.9 and 12.2 mg). In terms of Hoehn-Yahr's severity grade, severity increased in 20% of the patients undergoing bromocriptine monotherapy, whereas of the patients in the bromocriptine-levodopa combination group it was 45%. Wearing-off phenomenon was not seen in the bromocriptine monotherapy group. By contrast, 30% of the patients in the combination therapy group manifested this phenomenon which, when it occurred, invariably followed the administration of levodopa. Absence of the wearing-off phenomenon implies that bromocriptine has a direct protective action on degenerating substantia nigra.

Bromocriptine↗
PubMed1995

Effects of bromocriptine on cardiovascular regulation in healthy humans.

Bromocriptine, a dopamine agonist with central nervous system actions, may reduce sympathetic nervous system activity. We tested this hypothesis by measuring arterial blood pressure, central venous pressure, heart rate, muscle sympathetic nerve activity, and forearm blood flow before and after unloading the arterial baroreceptors with sodium nitroprusside (0.5 to 1.5 mcg/kg per minute IV), before and after unloading the cardiopulmonary baroreceptors with incremental lower body negative pressure (0 to -15 mm Hg), and before and after immersion of the hand in ice-cold water for 2 minutes (cold pressor test). After obtaining basal responses to provocative maneuvers, we gave 20 healthy subjects either 5 mg oral bromocriptine (n = 10) or placebo (n = 10) in a randomized, double-blind fashion. Bromocriptine did not affect resting mean arterial pressure, heart rate, or forearm blood flow. Bromocriptine decreased resting central venous pressure by 1.2 mm Hg (P < .05) and tended to increase total integrated muscle sympathetic nerve activity (from 151 +/- 44 to 212 +/- 82 U/min, P = NS). The reflex increases in muscle sympathetic nerve activity to nitroprusside infusion and lower body negative pressure were unchanged by bromocriptine; however, vascular responsiveness to both maneuvers was impaired after bromocriptine administration compared with control. Without bromocriptine, the reflex increase in muscle sympathetic nerve activity after nitroprusside-induced hypotension maintained forearm blood flow at a constant level, whereas with bromocriptine the forearm blood flow increased from 1.9 +/- 0.3 to 2.8 +/- 0.6 mL/min per 100 mL (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Centrally mediated effects of bromocriptine on cardiac sympathovagal balance.

Bromocriptine, a dopamine agonist, is known to lower cardiovascular mortality in L-dopa-treated patients with Parkinson's disease, probably by reducing the cardiac sympathetic activity. We aimed at unmasking the central effects of bromocriptine on the heart by power spectrum analysis. Ten healthy subjects (aged 31+/-2 years) in supine and sitting positions were evaluated after the administration of bromocriptine (2.5 mg) alone and after pharmacological peripheral D(2)-like blockade by domperidone (20 mg). We calculated (autoregressive method) the following: the low-frequency (LF) component (an index of cardiac sympathetic tone), the high-frequency (HF) component (an index of cardiac vagal tone), and the LF/HF ratio (an index of cardiac sympathovagal balance). With subjects in the supine position, bromocriptine alone induced a significant increase in the LF component and the LF/HF ratio, together with a reduction in norepinephrine plasma levels and blood pressure values. These conflicting effects can be explained as the combined result of direct and indirect (reflex-mediated) actions of bromocriptine in vivo. No changes in cardiac autonomic drive were observed with subjects in the sitting position. After domperidone pretreatment, bromocriptine induced a reduction in the LF component and in the LF/HF ratio. The sitting position caused an increase in heart rate and in the LF/HF ratio. We demonstrated both peripheral and central effects of bromocriptine. In particular, pretreatment with a peripheral antagonist (domperidone) allowed us to unmask the central effect of bromocriptine on cardiac sympathetic drive.

Adult↗
PubMedDate not supplied

Effects of bromocriptine on dopamine turnover with or without levodopa.

Bromocriptine, a dopamine agonist, alleviates symptoms of Parkinson's disease, even when administered alone, and is used for its treatment. Better therapeutic effects are, however, achieved when bromocriptine is used in combination with levodopa. In this study, we examined the biochemical changes caused by bromocriptine administration with and without levodopa, and evaluated the effects of the treatments on dopamine turnover in the mouse striatum. Results show that dopamine turnover is suppressed by the administration of bromocriptine alone with a slight decrease in the amount of dopamine, and dopamine turnover is very strongly promoted by the administration of levodopa. When the two drugs are administered together, bromocriptine enhances the levodopa-induced increase in dopamine turnover in the striatum. These findings indicate that bromocriptine therapy in combination with levodopa enhances the dopaminergic function and suggest that the combination therapy of bromocriptine and levodopa shows good efficacy. The results of this study may, thus, provide a theoretical basis for the combination therapy of bromocriptine and levodopa.

Analysis of Variance↗