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PubMed2002

Attenuation of working memory and spatial acquisition deficits after a delayed and chronic bromocriptine treatment regimen in rats subjected to traumatic brain injury by controlled cortical impact.

Cognitive impairments are pervasive and persistent sequelae of human traumatic brain injury (TBI). In vivo models of TBI, such as the controlled cortical impact (CCI) and fluid percussion (FP), are utilized extensively to produce deficits reminiscent of those seen clinically with the hope that empirical study will lead to viable therapeutic interventions. Both CCI and FP produce spatial learning acquisition deficits, but only the latter has been reported to impair working memory in rats tested in the Morris water maze (MWM). We hypothesized that a CCI injury would impair working memory similarly to that produced by FP, and that delayed and chronic treatment with the D2 receptor agonist bromocriptine would attenuate both working memory and spatial learning acquisition deficits. To test these hypotheses, isoflurane-anesthetized adult male rats received either a CCI (2.7 mm deformation, 4 m/sec) or sham injury, and 24 h later were administered bromocriptine (5 mg/kg, i.p.) or vehicle, with continued daily injections until all behavioral assessments were completed. Motor function was assessed on beam balance and beam walking tasks on postoperative days 1-5 and cognitive function was evaluated in the MWM on days 11-15 for working memory (experiment 1) and on days 14-18 for spatial learning acquisition (experiment 2). Histological examination (hippocampal CA1 and CA3 cell loss/survival and cortical lesion volume) was conducted 4 weeks after surgery. All injured groups exhibited initial impairments in motor function, working memory, and spatial learning acquisition. Bromocriptine did not affect motor function, but did ameliorate working memory and significantly attenuated spatial acquisition deficits relative to the injured vehicle-treated controls. Additionally, the injured bromocriptine-treated group exhibited significantly more morphologically intact CA3 neurons than the injured vehicle-treated group (55.60 +/- 3.10% vs. 38.34 +/- 7.78% [p = 0.03]). No significant differences were observed among TBI groups in CA1 cell survival (bromocriptine, 40.26 +/- 4.74% vs. vehicle, 29.13 +/- 6.63% [p = 0.14]) or cortical lesion volume (bromocriptine, 17.78 +/- 0.62 mm3 vs. vehicle, 19.01 +/- 1.49 mm3 [p > 0.05]). These data reveal that CCI produces working memory deficits in rats that are similar to those observed following FP, and that the delayed and chronic bromocriptine treatment regimen conferred cognitive and neural protection after TBI.

Animals↗
PubMedDate not supplied

Severe leukopenia and mild thrombocytopenia after chronic bromocriptine (CB-154) administration.

A 23-year-old woman was receiving bromocriptine (CB-154, 7.5-10 mg/day, for a hyperprolactinemic galactorrhea-amenorrhea syndrome. She also had insulin-dependent diabetes. After three months the bromocriptine therapy was stopped because she developed severe leukopenia (leukocyte counts about 1,800/cu mm) and mild thrombocytopenia (platelet count about 130,000/cu mm). Five months after stopping the bromocriptine therapy, the leukocyte count returned to normal (4,400/cu mm), as did the platelet count (238,000/cu mm). Prior to bromocriptine therapy, the patient's leukocyte and platelet counts ranged between 5,500 and 6,000/cu mm and 250,000 and 300,000/cu mm, respectively. While taking bromocriptine she was on insulin maintenance therapy and took no other drugs. Regular menses had returned and spontaneous galactorrhea had disappeared during bromocriptine therapy, and serum prolactin levels became normal. After stopping bromocriptine therapy the patient again became basally hyperprolactinemic and amenorrheic, with spontaneous galactorrhea. The article discusses possible mechanisms of this hematologic reaction.

Adult↗
PubMed1990

Bromocriptine and puerperal seizures.

Case reports have prompted concern that the use of bromocriptine mesylate to prevent lactation in the puerperium increases the risk of postpartum seizure. We conducted a record-based case-control study of postpartum seizures in three data bases to evaluate this relation. We identified 43 women who had a postpartum seizure, and we matched 319 controls individually by hospital of delivery, quinquenium of age, and time of delivery. Overall, women taking bromocriptine had a 22% lower risk for seizures, that is, the relative risk estimate was 0.78, with a 90% confidence interval of 0.29 to 1.87. A reduction in seizure risk is consistent with reports of antiseizure activity for bromocriptine in various species, including humans. We found a small positive association between bromocriptine use and seizures occurring more than 72 hours after delivery, with a relative risk estimate of 1.6 after controlling for seizure history. This association was offset by a strong negative association between bromocriptine use and early-occurring seizures. The pattern of an initial reduced risk followed by an increase to normal or above-normal levels of risk could result from an antiseizure activity of bromocriptine, with a rebound in risk when bromocriptine is withdrawn.

Adolescent↗
PubMedDate not supplied

Switching from bromocriptine to ropinirole in patients with advanced Parkinson's disease: open label pilot responses to three different dose-ratios.

Newly introduced dopamine agonists, such as ropinirole, may offer advantages compared to such older drugs as bromocriptine in patients with advanced Parkinson's disease (PD) with response oscillations or waning efficacy. Dose equivalence of these two drugs, however, has not been well established, which may complicate switching in clinical practice. In 23 such patients with advanced PD no longer satisfactorily responsive to prolonged bromocriptine therapy (mean dose: 18.9 +/- 6.5 mg/d), we prospectively switched the medication to ropinirole administered at three different dose-ratios (5:1, 3:1, and 2:1), increased at monthly intervals. Selegiline remained unmodified in all 17 patients receiving this medication. A dose-ratio of bromocriptine to ropinirole of close to 2:1 (1.87; mean ropinirole dose: 10.1 +/- 2.5 mg/d) was the only dose that significantly reduced mean motor Unified Parkinson's Disease Rating Scale (UPDRS) scores ( p = 0.030, analysis of variance). Individually considered, however, four patients (21%) scored worse even at this dose-ratio when compared to baseline assessment on bromocriptine. "Off" time was reduced by 57.3% in fluctuating patients, and the dyskinesia score decreased by 53.8%, although the changes were not statistically significant. Higher bromocriptine to ropinirole dose ratios (i.e., 5:1 and 3:1) resulted in "off"-time increases in half of the patients with fluctuations, and two previously stable patients developed a wearing-off effect and one other patient experienced off-time dystonia. One patient developed dose-dependent dopaminomimetic psychotic symptoms with ropinirole. In conclusion, "off"-time motor scores and possibly "off"-time duration, and severity of dyskinesias in patients with advanced PD with prolonged bromocriptine therapy may improve in a majority of cases by switching to ropinirole, provided that the latter drug is administered at a dose ratio of 2:1 compared to bromocriptine. Higher dose ratios are often ineffective or may even cause a clinical worsening of symptoms in some patients.

Adult↗
PubMedDate not supplied

Effect of bromocriptine on cardiac function and coronary blood flow.

The present study was designed to investigate the effects of bromocriptine, a dopamine receptor agonist, on systemic and coronary hemodynamics and to determine the mechanisms involved in the action of this compound. Intravenous infusion of bromocriptine (1 microgram/kg/min for 20 min) to pentobarbital-anesthetized dogs produced significant decreases in blood pressure, heart rate, total peripheral resistance, peak dP/dt, left ventricular pressure, and coronary blood flow. There were significant increases in stroke volume and coronary vascular resistance, whereas the index of contractility was unaffected. Cardiac output was decreased 30 min after the termination of bromocriptine infusion. The cardiovascular actions of bromocriptine were significantly antagonized by the dopamine receptor antagonist, sulpiride. Bromocriptine also failed to exert these effects when administered to animals that were treated with ganglionic blocking agents. These results suggest that the hypotensive action of bromocriptine is mainly due to a decrease in total peripheral resistance. In addition, the actions of bromocriptine on cardiac function are the result of activation of presynaptic dopamine receptors and the drug does not have any direct action on the myocardium.

Animals↗
PubMed1979

Bromocriptine treatment of oligospermia: a double blind study.

A double blind controlled study of bromocriptine treatment of oligospermia was carried out. Out of fifty-one men who originally volunteered to the study there were forty who took the drug for 12 weeks as requested. All the partners of these men had failed to conceive, and in each case the pretreatment sperm count had been below 40 million/ml on two or several occasions. The pretreatment serum prolactin concentrations were similar in patients given bromocriptine (N = 20) and placebo (N = 20). There were three men in either group whose pretreatment serum prolactin concentration was in excess of 30 micrograms/l, the highest value being 96 micrograms/l. While bromocriptine effectively decreased the serum prolactin concentration, it had no significant effect over placebo on sperm volume, motility and morphology. In the bromocriptine group, sperm count increased to or above 40 million/ml in five out of twenty men, while in the placebo group this occurred in nine out of twenty patients. The plasma testosterone and dihydrotestosterone levels increased slightly during treatment in both groups, but no significant difference was observed between bromocriptine and placebo treated patients. One wife of a bromocriptine-treated man and two wives of placebo-treated men became pregnant during treatment. In this study bromocriptine was no more effective than placebo in the treatment of oligospermia.

Adult↗
PubMed1987

Effect of bromocriptine on LH pulsatility in the polycystic ovary syndrome.

The effects were studied of bromocriptine, 10 mg daily for 1 year, on luteinizing hormone (LH) pulse characteristics in patients with classical polycystic ovarian syndrome (PCOS). All patients were hirsute, had been oligomenorrhoeic since menarche, had LH: FSH ratios of greater than 3:1, and either elevated serum testosterone (T) or dehydroepiandrosterone sulphate (DHAS) concentrations. In 10 subjects who completed the study menstrual frequency increased from an average of 3.6 to 8 per year but few of the cycles were ovulatory. Mean (SE) serum testosterone fell from 4.4 (0.5) nmol/l pretreatment to 2.8 (0.3) nmol/l (P less than 0.01) and DHAS from 7.9 (1.1) mumol/l to 5.4 (1.1) mumol/l (P less than 0.05). Serum delta 4 androstenedione and oestradiol did not change with bromocriptine treatment. Mean serum LH fell from 17.4 (2.4) IU/l to 11.2 (1.8) IU/l (P less than 0.03) after 12 months of bromocriptine. No pattern of LH pulsatility specific to PCOS was detected during 10 min sampling for an 8 h period prior to dopamine agonist treatment. LH interpeak interval (58 (5.2) min) and peak amplitude (156 (7.2%) of mean nadir) in untreated PCOS were similar to that of the mid-follicular stage of ovulatory cycles, and bromocriptine for 1 year did not alter these variables. We conclude that while bromocriptine reduces serum androgen levels and increases menstrual frequency it has no effect centrally to modify hypothalamic GnRH secretion. The reduction in LH levels by bromocriptine may be the result of diminished gonadotroph sensitivity to GnRH or reduced pituitary stores of LH available for release. Despite the return towards normal of various hormonal characteristics of PCOS, bromocriptine has little place in the management of this condition.

Adolescent↗
PubMed1983

Pituitary responsiveness to LHRH and TRH in men: effect of bromocriptine and clomiphene treatment.

The effect of the concomitant use of bromocriptine and clomiphene on pituitary function was tested in 8 healthy men, who ingested either 100 mg of clomiphene, 5 mg of bromocriptine or 100 mg of clomiphene +5 mg of bromocriptine daily for 7 days. Plasma concentrations of FSH and LH increased similarly during clomiphene and clomiphene + bromocriptine intake. Bromocriptine decreased the plasma levels of prolactin (Prl) and this decrease was unaffected by clomiphene. The latter blunted the plasma LH response to LHRH whilst bromocriptine blunted the Prl response to TRH, but Clomiphene and bromocriptine together had no additive effects on gonadotrophin and Prl secretion. It thus seems likely that this combination offers no advantage over clomiphene alone in the treatment of normoprolactinaemic infertile men.

Adult↗
PubMed1985

Long-term bromocriptine therapy may restore the inhibitory control of prolactin release in some patients with pathological hyperprolactinemia.

While bromocriptine is effective in controlling hyperprolactinemia, it is not known if bromocriptine therapy can restore the abnormal regulation of prolactin (PRL) release found in patients with pathological hyperprolactinemia. We report 15 hyperprolactinemic patients treated for a mean duration of 5.5 +/- 0.6 years (mean +/- SE) in whom stimulation tests to assess PRL control mechanisms [thyrotropin releasing hormone (TRH) and metoclopramide] were performed before and at least one month after withdrawal of bromocriptine therapy. The basal PRL level after withdrawal of bromocriptine therapy was significantly lower (p less than 0.001) than that before therapy. All patients had blunted PRL stimulatory responses to TRH and metoclopramide (% delta 16.0 +/- 5.6%) before treatment. After withdrawal of bromocriptine, PRL responses to stimulatory tests were significantly improved in seven patients (termed 'responders', % delta 376 +/- 55%) but remained unchanged in eight patients (termed 'non-responders', % delta 9.2 +/- 3.0%). Basal PRL levels were significantly lower (p less than 0.01) in responders (290 +/- 35 mIU/l) than in non-responders (10360 +/- 6790 mIU/l). Four of the responders have maintained normoprolactinemia and normal stimulated PRL responses for 15 months to three years following cessation of bromocriptine therapy and appear to be in remission. Favourable factors amongst the responders were the female sex, absence of a macroadenoma, and a pre-treatment PRL level below 3000 mlU/l. PRL stimulation tests performed before therapy could not predict which patients would respond. No relationship was found between duration of therapy, or age at presentation, and improvement after bromocriptine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1990

Effect of bromocriptine on neurogenic vasoconstriction in the isolated autoperfused hindquarters of the rat.

The effects of local administration of bromocriptine were studied in the isolated autoperfused hindquarters of the rat, and compared to the actions of apomorphine and pergolide. Local injection of bromocriptine (1 microgram kg-1) (into the hindquarters) did not alter perfusion pressure, but reduced the pressor response to electrical stimulation of the lumbar sympathetic chains at all frequencies used (0.5-10 Hz; 5 ms; 35 V). Bromocriptine (1 microgram kg-1) did not alter the increases in perfusion pressure induced by local administration of noradrenaline. The effects of local administration of apomorphine (1 microgram kg-1) and pergolide (1 microgram kg-1) were similar to that of bromocriptine. The inhibitory effect by bromocriptine, apomorphine and pergolide of the stimulation-evoked pressor responses was completely antagonized by intravenous administration of the dopamine receptor antagonist sulpiride (0.3 mg kg-1) but was not by the alpha 2-adrenoceptor antagonist yohimbine (1 mg kg-1). In this dose, yohimbine antagonized the inhibitory effect of the alpha-adrenoceptor agonist clonidine (1 microgram kg-1). The inhibitory effect of clonidine was not altered by sulpiride but was antagonized by yohimbine. The results indicate that bromocriptine like apomorphine and pergolide inhibit neurally-induced pressor responses in the autoperfused hindquarters of the rat by stimulation of presynaptic dopamine receptors. Stimulation of these receptors leading to a fall in noradrenaline release and consequently of vasomotor tone, might at least in part explain the vasodilatator effects of bromocriptine in the rat.

Animals↗
PubMed1990

Cardiovascular effects of bromocriptine in rats: role of peripheral adrenergic and dopaminergic receptors.

1. Experiments were designed to study the involvement of alpha-adrenoceptors and dopamine receptors in the hypotensive and bradycardic actions of bromocriptine in rats. 2. Intravenous administration of bromocriptine reduced blood pressure and heart rate which was inhibited by ganglionic blocking agents or by pithing. 3. The fall in blood pressure produced by bromocriptine was not modified by atropine, atenolol, prazosin, yohimbine, bilateral vagotomy or carotid ligation, but was blocked by sulpiride, domperidone and haloperidol. 4. The bradycardia produced by bromocriptine in intact rats was assumed to be mediated by the autonomic nervous system since it was partly reduced by bilateral vagotomy or atenolol, and entirely prevented by pithing. Furthermore, sulpiride but not yohimbine antagonized this effect. 5. In pithed rats, bromocriptine decreased both the pressor response (above 10 micrograms kg-1) and the tachycardia (above 50 micrograms kg-1) elicited by electrical stimulation of spinal cord outflow. Both effects were inhibited by sulpiride or yohimbine. 6. In pithed rats, bromocriptine did not affect the hypertension due to exogenous noradrenaline, phenylephrine, B-HT 920, nor the bradycardia evoked by stimulation of the cardiac muscarinic receptors by carbachol. 7. These results suggest that, in rats, bromocriptine produces hypotension via an action on presynaptic and/or ganglionic dopamine receptors, and causes bradycardia by activation of central dopamine receptors.

Anesthesia↗
PubMed1990

Bromocriptine blood levels after the concomitant administration of levodopa, amantadine and biperiden in Parkinson's disease.

We recently demonstrated that when different drugs (mainly used for the treatment of Parkinson's disease) are administered in combination they interfere with the availability of bromocriptine in the brain of rats (striatum and hypothalamus). In the present study performed with parkinsonian patients, we measured plasma levels of bromocriptine (RIA) over 4 h after giving orally 5 mg bromocriptine alone; together with levodopa 250 mg plus 25 mg DCI (10 patients); with 100 mg amantadine HCl (5 patients) and with biperiden 5 mg (5 patients). Amantadine and biperiden did not interfere with the pharmacokinetics of bromocriptine. However, levodopa significantly diminished plasma levels (a mean increment of 1.78 mg +/- 0.30 vs 0.92 +/- 0.18 mg/ml). We postulate that levodopa may interfere with the metabolism of bromocriptine in the liver. Although we did not observe substantial clinical differences among the patients (Webster scale), this study supports our previous findings and suggests that one of the advantages of 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 availability and enables a more "stable" penetrability of the medication into the central nervous system.

Administration, Oral↗
PubMed1984

Failure of amantadine and bromocriptine to counteract alcoholic inebriation in man.

Oral amantadine 100 mg and bromocriptine 2.5 + 2.5 mg, alone and in combination with ethanol (1 g/kg), were investigated in two placebo-controlled, double-blind and cross-over trials. In the first trial the psychomotor effects of amantadine and bromocriptine were compared to those of placebo, and in the second trial ethanol was added to the treatment. Bromocriptine lowered serum prolactin levels, thus confirming its absorption. Amantadine and bromocriptine alone had no psychomotor effects but unpleasant sensations, nausea and dizziness were reported after bromocriptine. Ethanol impaired performance in terms of impaired coordinative and reactive skills, lowered tapping speed, prolonged critical flicker interval and reduced gaze nystagmus angle (P less than 0.05 to 0.001; two-way ANOVA). Subjectively, ethanol induced mental slowness, clumsiness and impairment of performance (P less than 0.05 to 0.001). Amantadine and bromocriptine failed to counteract any of these ethanol-induced changes. It is concluded that in man, an acute dopaminergic activation by amantadine or bromocriptine does not significantly modify the psychomotor effects of ethanol.

Adult↗
PubMed1985

Enhanced depressor effect of bromocriptine in the DOCA/NaCl hypertensive rat.

To elucidate the role of the dopaminergic system in the maintenance of hypertension in the deoxycorticosterone acetate (DOCA)/NaCl hypertensive rat, the responses of mean arterial pressure (MAP), plasma norepinephrine (NE), epinephrine (E), and prolactin (PRL) to intravenous (iv) administration of bromocriptine, a dopamine agonist, and hexamethonium bromide, a ganglion blocker, were examined in conscious, unrestrained 4-wk DOCA/NaCl hypertensive rats. Bromocriptine was administered to adrenomedullectomized (ADMX) rats to assess the role of the adrenal medulla in its depressor effect. Bromocriptine (50, 250, and 500 micrograms/kg) and hexamethonium (3 and 30 mg/kg) caused dose-dependent decreases in MAP that were greater in DOCA/NaCl rats than in uninephrectomized controls. Basal plasma NE, E, and PRL were significantly higher in DOCA/NaCl rats than in controls. Bromocriptine (500 micrograms/kg iv) decreased plasma PRL to undetectable levels and increased plasma E significantly without changing NE levels in DOCA/NaCl and uninephrectomized control rats. In ADMX rats bromocriptine (500 micrograms/kg iv) decreased MAP, PRL, and NE without affecting E levels. These results suggest that the depressor response to bromocriptine could be related to inhibition of sympathetic outflow without participation of the adrenal medulla. The hyperprolactinemia and enhanced depressor response to bromocriptine observed in DOCA/NaCl animals suggest that the dopaminergic system might be altered in this model of hypertension.

Adrenal Medulla↗
PubMed2001

Pregnancy in hyperprolactinemic infertile women treated with vaginal bromocriptine: report of two cases and review of the literature.

Vaginal bromocriptine has proven safe and effective in treating hyperprolactinemic women. However, there has been no long-term clinical assessment regarding the influence of daily vaginal bromocriptine administration on the ability to conceive. This article presents two cases of successful pregnancy resulting from this alternative treatment. An infertile woman with an empty sella and hyperprolactinemia was treated with vaginal bromocriptine because of intolerance to oral administration. Prolactin levels were quickly normalized and no side effects occurred. Repeated postcoital tests during treatment proved normal. Twelve months later, the patient conceived. The therapy was discontinued during pregnancy, without complications. Although bromocriptine treatment was not resumed after delivery, postpartum prolactin levels were lower than before treatment and magnetic resonance imaging revealed an unchanged empty sella. Another patient with infertility and pituitary microadenoma with intolerance to oral dopaminergic agonists received the same treatment. Prolactin quickly fell to within the normal range. Vaginal bromocriptine was well tolerated and postcoital test results were not impaired. Tumor regression occurred and 10 months later the patient conceived. Despite bromocriptine withdrawal, no significant complications occurred during pregnancy. It can therefore be concluded that a couple's fertility does not appear to be significantly affected by the persistent local presence of bromocriptine.

Adenoma↗
PubMed1992

Differential inhibition of dopamine and bromocriptine on induced prolactin release: multiple sites for the inhibition of dopamine.

Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 +/- 0.5 to 151.2 +/- 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/l) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D2 receptor transduction system.

Animals↗
PubMed1989

Bromocriptine alters hormone rhythms and lipid metabolism in swine.

Hormones, metabolites and activities involved in lipid synthesis were assayed in pigs made leaner by bromocriptine treatment. Market size female swine were allowed free access to food under natural lighting conditions and implanted with bromocriptine pellets designed to release 10 mg/pig/day for 28 days in an effort to inhibit prolactin secretion. Between the 2nd and 3rd week of treatment, plasma samples were obtained from each group at 4-hour intervals throughout the day for assays of prolactin, cortisol, insulin, triglyceride, cholesterol and glucose concentrations. Twenty-eight or thirty days after the implantations, all animals were sacrificed for determinations of backfat thickness and insulin binding in the liver. At sacrifice, bromocriptine treatment reduced backfat thickness by 14% and insulin binding to partially purified hepatic membranes by 39% compared with control values. At 14 days following implantations, there were dramatic daily variations in plasma cortisol and prolactin levels in the control pigs and these rhythms were markedly altered in phase and amplitude in the bromocriptine-treated pigs. Bromocriptine reduced by 45, 20 and 13% the high levels of triglyceride, glucose, and cholesterol, respectively, that were found in control pigs near sunset. Plasma insulin concentrations did not vary during the day in control pigs and bromocriptine did not influence the insulin levels. The findings support important roles for a temporal synergism of cortisol and prolactin rhythms in maintaining hepatic lipogenic responsiveness to insulin. Bromocriptine treatment alters these hormonal relations and reduces lipid synthesis.

Animals↗
PubMed1991

A giant prolactinoma and the effect of chronic bromocriptine therapy on basal and TRH-stimulated serum prolactin levels.

The role of bromocriptine as primary therapy for prolactin-producing tumors is currently well accepted in the literature. Bromocriptine decreases the concentration of serum prolactin and this decrease precludes tumor shrinkage, despite the lack of correlation between amount of decrease in tumor size and baseline serum prolactin. We submit the case of a patient on chronic bromocriptine therapy followed by measuring baseline and thyrotropin-releasing hormone (TRH)-stimulated serum prolactins. Bromocriptine affects both release and storage of prolactin. The literature has suggested that the effects of bromocriptine on storage and synthesis may be responsible for its effects on tumor size. It was felt that TRH stimulation would more accurately reflect storage and synthesis, and thus correlate better with tumor size. The pituitary was initially debulked via a right frontal approach; then the patient was placed on bromocriptine therapy and postoperatively followed with baseline and TRH-stimulated serum prolactins. The size of the pituitary was measured by computed tomography. Baseline serum prolactin levels rapidly decreased, but despite the slow decrease in TRH-stimulated prolactins no change was noted in tumor size. Because of the time difference between the baseline and TRH-stimulated prolactin levels, we conclude that clinically bromocriptine affects primarily secretion of prolactin and secondarily storage and synthesis. We also show that TRH-stimulated prolactin does not correlate with size of prolactin-secreting pituitary tumors and therefore tumor size should be independently measured. The literature has shown that prolactinomas do not respond well to TRH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Bromocriptine↗