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PubMed1986

[Polycystic ovary--classification and treatment by bromocriptine].

Plasma levels of androstenedione (A) and dehydroepiandrosterone sulfate (DHAS) were measured in 29 women with PCO in an attempt to classify PCO. A and/or DHAS were elevated in all cases. In cases with DHAS levels below 2,000 ng/ml, the A levels were found to be over 1.4 ng/ml. This group was defined as an ovarian type because the major source of A is the ovary. In contrast, women whose DHAS levels were higher than 2,000 ng/ml were classified as an adrenal type. In both groups, the hormonal features were elevated LH levels and exaggerated LH response to LHRH. The mean A levels were 2.43 +/- 0.31 ng/ml in ovarian type and 2.20 +/- 0.42 ng/ml in adrenal type. The mean DHAS levels for the adrenal type were 3,052 +/- 299 ng/ml, or about 3 times as high as normal values. On the other hand, those for the ovarian type were on the upper borderline of the normal range. In both groups, dexamethasone lowered DHAS levels by about 80% with no discernible effect upon A levels. The successful rate for ovulation-induction by clomiphene was 20% in the ovarian and 33% in the adrenal. Bromocriptine induced ovulation in 8 out of 9 cases of the ovarian type. However, only one of 6 responded to bromocriptine in the adrenal type. Bromocriptine-unresponsive cases of the adrenal type ovulated following treatment with combination of clomiphene and prednisolone. In summary, we attempted to classify PCO into ovarian and adrenal types by analyzing the elevated androgen level. This classification seems to be useful in the treatment of PCO and also provides some insight into the pathogenesis of PCO.

Adolescent↗
PubMedDate not supplied

Antagonism of bromocriptine-induced cage climbing behaviour in mice by the selective D-2 dopamine receptor antagonists, metoclopramide and molindone.

Bromocriptine (5-30 mg/kg, ip), 2 hr after administration, induced cage climbing behaviour in mice. Pretreatment with haloperidol, an antagonist of both D-1 and D-2 dopamine receptors, metoclopramide and molindone, the selective D-2 dopamine receptor antagonists, effectively antagonised bromocriptine-induced climbing behaviour. The results indicate that bromocriptine most probably induces climbing behaviour in mice by stimulating the postsynaptic striatal D-2 dopamine receptors.

Animals↗
PubMed1987

The influence of bromocriptine on the ultrastructure of the biceps femoris muscle in mice.

Bromocriptine and other dopaminergic agonists drugs are used in Parkinson's disease. In this paper we have studied the ultrastructure of striated muscle of mice after bromocriptine treatment. There was a tremendous increase in the number and size of mitochondria, as well as a very notable increase in the cristae. Some ultrastructure changes were also noted at the neuromuscular junctions. An explanation has been attempted in the light of other investigations concerning the relationship of microtubules and bromocriptine on the one hand, and microtubules and mitochondria on the other.

Animals↗
PubMed1985

Neuronal and postjunctional components in the blood pressure effects of dopamine and bromocriptine in rabbits.

We have studied the contribution of neuronal and postjunctional dopamine (DA) receptors and of the DA1 and DA2 receptor subtypes to the blood pressure effects of DA and bromocriptine in the rabbit. The norepinephrine release rate, i.e., the rate of entry of endogenous norepinephrine into the plasma, was derived from the plasma level of endogenous norepinephrine and the plasma [3H]norepinephrine clearance. Bromocriptine (40 micrograms kg-1) lowered the norepinephrine release rate and the arterial blood pressure both in anesthetized rabbits and in pithed rabbits with electrically stimulated sympathetic outflow. These effects were antagonized by the selective DA2 antagonist domperidone but not by the selective DA1 antagonist SCH 23390. DA (10-160 micrograms kg-1 min-1) dose-dependently increased the norepinephrine release rate and caused only transient hypotension in anesthetized rabbits. However, after treatment with desipramine, DA did not change the norepinephrine release rate and produced a persistent fall in blood pressure. When DA and domperidone were given simultaneously to desipramine-treated rabbits, the hypotensive effect of DA was unchanged, but now DA increased the norepinephrine release rate. When DA and SCH 23390 were given simultaneously to desipramine-treated rabbits, DA failed to lower blood pressure and decreased the norepinephrine release rate. Propranolol did not change the effects of DA in desipramine-treated rabbits. These results suggest that bromocriptine decreases blood pressure by activating ganglionic and/or prejunctional, inhibitory DA2 receptors in the peripheral sympathetic nervous system. DA also activates these receptors, but in addition releases norepinephrine in the manner of an indirectly acting sympathomimetic amine and activates postjunctional vascular DA1 receptors, and the latter seems to be the main component in DA-induced hypotension.

Anesthesia↗
PubMed1987

Prolonged suppression of a corticotropin-producing bronchial carcinoid by oral bromocriptine.

The addition of orally administered bromocriptine mesylate to cyproheptadine hydrochloride therapy completely normalized urinary-free cortisol levels for three months in a 21-year-old woman with Cushing's syndrome in whom results from standard dexamethasone suppression and metyrapone stimulation tests as well as baseline corticotropin levels were originally compatible with a diagnosis of an occult pituitary adenoma. When transsphenoidal exploration of the sella turcica was unsuccessful and hypercortisolism persisted, the source of corticotropin was discovered using petrosal sinus and venal caval catheterization. A 1 X 1.5-cm carcinoid tumor of the lung was identified and removed, thereby correcting the hypercortisolism. The tumor was demonstrated by immunoperoxidase staining to contain corticotropin. Orally administered bromocriptine, with or without cyproheptadine therapy, may be useful in the palliative treatment of some patients with carcinoid or other ectopic corticotropin-producing tumors. We postulate that bromocriptine therapy acted directly on carcinoid tumor cells to directly inhibit corticotropin production by a dopaminergic mechanism.

Administration, Oral↗
PubMedDate not supplied

[Value of cyclofenil in the inhibition of lactation. Efficacy compared to bromocriptine].

The inhibitory effects of cyclofenil and bromocriptine on lactation as well as FSH, prolactin and estradiol levels have been compared in control and treated females. The clinical activity of cyclofenil was lower than that of bromocriptine but was virtually free of side-effects. Cyclofenil and bromocriptine only presented similar hormonal effects at the 20th day ; this suggests that the mechanism of action of cyclofenil is more linked to secondary increases in estrogen levels than to a primary effect. Cyclofenil is of particular value in cases of vascular hypersensitivity yo ergot derivatives and for toxemic patients treated with beta-blockers.

Adult↗
PubMed1988

Suppression of lactation. A comparison of bromocriptine and prostaglandin E2.

Women in the puerperium who requested lactation suppression were randomly allocated to receive bromocriptine from puerperal day 1 to 14 or prostaglandin E2 from day 3 or 4 for 24 hours. Subjectively, lactation suppression was satisfactory in all cases. Objective measurements showed a trend toward more-effective early suppression with bromocriptine. After discharge from the hospital, 3 of the 21 women who received prostaglandin E2 complained of mild breast tenderness, whereas 10 of the 22 who received bromocriptine reported severe "rebound" breast tenderness.

Bromocriptine↗
PubMed1988

A double-blind study of bromocriptine and L-dopa in de novo Parkinson's disease. Short-term results.

The first phase of a longitudinal multicenter study comparing bromocriptine and L-dopa (as Sinemet) as de novo therapy for Parkinson's disease using a double-blind randomized design has recently been completed. Over a period of 5.5 months, bromocriptine and L-dopa were equipotent in reducing functional and neurological disability. These observations complement and extend earlier studies and suggest a role for bromocriptine as de novo therapy of Parkinson's disease.

Aged↗
PubMed1987

Low-dose bromocriptine in the early phases of Parkinson's disease.

The effect of bromocriptine at doses up to 20 mg/day was studied in a single-blind format with a placebo phase in 15 Parkinson's disease patients with mild-to-moderate disability who had not been previously treated with levodopa. For the 11 patients who completed the 9 month trial, both Northwestern University Disability Scale and Columbia University Rating Scale scores were significantly reduced during bromocriptine therapy, when compared with either baseline or placebo scores. Two patients improved greater than 50% and had no side effects. Transient side effects appeared in four patients. Bromocriptine at doses of 20 mg/day or below may yield effective symptomatic improvement in de novo parkinsonism and may be considered as the initial treatment in young parkinsonian patients with only mild-to-moderate disability.

Adult↗
PubMed1988

Prolactin stimulation tests: different response patterns after bromocriptine, lisuride, and metergoline treatment of puerperal women.

To elucidate different mechanisms by which bromocriptine, lisuride, and metergoline may inhibit prolactin (PRL) secretion and lactation in puerperal women, the PRL secretion patterns were examined by means of a stimulation test using an intravenous bolus of metoclopramide. After seven and 14 days of treatment, no significant difference in basal serum PRL levels was observed. However, women subjected to metergoline treatment had significantly higher responses of PRL to metoclopramide as compared with those treated with either bromocriptine or lisuride. Thus, the PRL-lowering mechanism of metergoline appears to be different from those of bromocriptine and lisuride.

Adult↗
PubMed1977

Bromocriptine versus placebo in levodopa treated patients with Parkinson's disease.

Twenty patients with idiopathic parkinsonism who had been on optimal levodopa therapy for at least 3 months prior to the investigation and where effect of the treatment was decreasing or side effects were increasing, were treated with bromocriptine in a double-blind crossover trial during a 12 + 12 weeks period. Reduction in disability scores was found significant. Hyperkinesia was more frequent in the bromocriptine period than in the placebo period, but reduction of dose in six patients for this reason was not followed by deterioration. Both hyperkinesia and other side effects disappeared after dose reduction. Doses were 2.5 mg-40 mg. Bromocriptine seems a valuable supplement to previous therapy in these patients.

Aged↗
PubMed1988

[Effect of bromocriptine on cerebral blood flow in Parkinson's disease].

We measured regional cerebral blood flow (CBF) with single photon emission computed tomography and Xenon 133 in 8 patients with Parkinson's disease (stages I or II) before and after acute oral administration of 10 mg bromocriptine. Moreover, Columbia University Rating scale and neuropsychological tests were assessed before and after drug administration. Bromocriptine induced a significant (p less than 0.01) increase in CBF (+ 12 p. 100) in all the regions studied unrelated to pCO2 variations. The Columbia motor scale score decreased (by 16 p. 100) whereas those on the neuropsychological tests did not vary. There was no relationship between the improvement in motor performance and the increase in CBF. The results suggest that the effect of bromocriptine on CBF is not mediated by an action on the major dopaminergic pathways in the brain but rather by a direct effect on dopaminergic receptors located on cerebral vessels.

Administration, Oral↗
PubMed1978

Inhibition of puerperal lactation by bromocriptine.

Puerperal lactation is regulated by a complex of hormones, including in particular prolactin. In a few instances prevention of lactation is desirable on medical grounds. However, most Western-European women who do not nurse their babies choose not to do so for personal reasons. In two double-blind studies the effect of bromocriptine was compared with that of placebo and an oestrogen/androgen compound. Bromocriptine prevented both milk secretion and engorgement of the breasts very effectively. It is clearly a better and more specific inhibitor of lactation than the combined oestrogen/androgen compound. Its effect is through the blockade of pituitary prolactin release. As normoprolactinaemia is reached, normal ovarian function is restored in bromocriptine treated women. To prevent the occurrence of a rebound lactation phenomenon, the drug has to be administered continuously for at least a fortnight.

Bromocriptine↗
PubMed1978

Acromegaly--results of long term treatment with bromocriptine.

Bromocriptine, a long acting dopamine agonist, has been used to treat 73 patients with active acromegaly for between 3 and 25 months. Clear clinical improvement occurred in 71 patients (97%). This included improvement in facial appearance, reduction in hand and foot size and sweating, relief of headaches and increased energy and libido. Abnormal visual fields became normal in two patients, but one of these was given concomitant radiotherapy. A significant reduction in growth hormone occurred in 58 patients (79%), but only 15 patients had levels persistently below 5microgram/l. Carbohydrate tolerance improved with the reduction in growth hormone and of 23 patients with diabetes mellitus before treatment, glucose tolerance became normal in 15 and improved in a further 5. Administration of bromocriptine should begin slowly in order to minimise early side effects. Long term side effects have been minor to date and the deaths of two patients whilst taking the drug were not considered to have been caused by it. Bromocriptine offers a major advance in the management of acromegaly, but further careful follow-up is required to determine whether serious side effects will be a problem with the long term use of high doses.

Acromegaly↗
PubMed1978

Bromocriptine therapy in patients with acromegaly: effects on growth hormone, somatomedin A and prolactin.

Six of ten patients were subjectively improved by bromocriptine treatment as illustrated by diminished sweating, reduction of soft tissue swelling and restoration of sexual potency and menstruations. These six patients had elevated or normal blood levels of prolactin, which could be stimulated by TRH and inhibited by bromocriptine. During medication two clinical responders normalized and one lowered plasma GH concentrations. Three clinical responders with initially increase somatomedin A levels normalized these levels during treatment, in one case despite lack of effect on GH levels. The four nonresponders had undetectable or notably depressed levels of prolactin, which could not be stimulated by TRH. It is suggested that the presence of prolactin, per se or as an indication of a certain dopaminergic situation, is a prerequisite for successful bromocriptine treatment of patients with acromegaly.

Acromegaly↗
PubMed1987

Does treatment with bromocriptine influence the course of hyperprolactinaemia?

Twenty-two women with hyperprolactinaemia without evidence of microadenoma, either untreated (n = 3), treated with bromocriptine for a total of less than 1 year (n = 12), or treated with bromocriptine for a total of more than 1 year (n = 7) were followed up by retrospective case-note review for at least 53 months. More than 50% of the women showed a fall in serum prolactin concentrations by more than 40% over the period of follow-up. The occurrence of a fall did not appear to be related to either length of treatment with bromocriptine or to the occurrence of pregnancy. Some women elected to remain untreated, despite symptoms, in preference to taking tablets and having to use contraception. The wisdom of leaving patients untreated in the light of these findings is discussed.

Adult↗
PubMed1987

[Antitumor effect of bromocriptine on estrogen-induced rat prolactinomas: special reference to changes in secretory granules by stereological analysis].

Bromocriptine (CB) not only lowers serum prolactin (PRL) levels but also reduces tumor size of human prolactinomas. Gen et al and we have suggested that the size reduction of human prolactinomas by bromocriptine treatment results from the reduction in size of individual tumor cell as well as the reduction in number of tumor cells secondary to cell necrosis. This implies that bromocriptine has a cytosuppressive action and possibly a cytocidal action on human prolactinomas which causes reduction in cell size and cell necrosis, respectively. The mechanism of cytosuppressive action of CB has been investigated by using mostly non-neoplastic pituitary tissues of experimental animals. A decrease in exocytosis of secretory granules and a subsequent accumulation of granules within the cells are suggested to cause the reduction in serum levels of PRL in early stage of CB treatment. However we have reported that in spite of a pronounced reduction of serum PRL levels, the number of exocytosis of the granules in human prolactinomas treated with CB for 2 weeks increased to more than 4 times much as that in the untreated prolactinomas. This is a phenomenon which contradictory to the current hypothesis. The present study is intended to clarify whether the phenomenon we observed is specific for human prolactinomas or common also to the prolactinomas in experimental animals. Seventeen female SD rats were used. They were implanted subcutaneously with a pellet of 20 mg of 17 estradiol-benzoate (20% in cholesterol), and left to grow a pituitary tumor for 10 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Treatment of hepatorenal syndrome with dopamine and bromocriptine].

Two cirrhotic patients with hepatorenal syndrome were treated with Dopamine hydrochloride and Bromocriptine, a Dopamine agonist. Dopamine hydrochloride was given at a dosis of 0.30 to 0.90 mg/min. and Bromocriptine 15 mg/day. Although a transient raise of urinary output was observed in one patient, both patients died six to ten days later with an urinary output of less than 100 ml/day. Dopamine and Bromocriptine combined are of poor therapeutic value in hepatorenal syndrome.

Adult↗