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Parlodel

Generic Parlodel is the most effective preparation in struggle against female diseases as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Generic Parlodel can also be helpful for patients with Parkinson`s disease and its symptoms caused by low levels of dopamine in the brain. Generic Parlodel acts as up-to-date remedy reducing prolactin level.

Other names for this medication:

Similar Products:
Apokyn, Mirapex, Requip

 

Also known as:  Bromocriptine.

Description

Generic Parlodel is created using perfect medical formula which is a magnificent weapon against women problems such as persistent breast milk production, infertility, amenorrhea (lack of a menstrual period) and other disorders caused by prolactin-secreting tumors. Target of Generic Parlodel is to reduce prolactin level and help to produce breast milk and fertility in women.

Generic Parlodel acts as up-to-date remedy reducing prolactin level. When it is used for treatment of Parkinson disease, it works by stimulating dopamine receptors in some certain brain parts.

Parlodel is also known as Bromocriptine, Proctinal.

Generic Parlodel is a hormone (dopamine agonist).

Generic Parlodel can't lead to vaginal bleeding, uterine or breast cancer, breast tenderness.

Generic name of Generic Parlodel is Bromocriptine.

Brand name of Generic Parlodel is Parlodel.

Dosage

Generic Parlodel is available in the form of tablets (2.5 mg) which should be taken by mouth with meals or without it.

Take Generic Parlodel every day at the same time and remember that its dosage depends on patient's health state.

If you want to achieve most effective results do not stop taking Generic Parlodel suddenly.

Overdose

If you overdose Generic Parlodel and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store below 25 degrees C (77 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

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The most common side effects associated with Parlodel are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Parlodel if you are allergic to Generic Parlodel components.

Do not take Generic Parlodel if you are pregnant, planning to become pregnant or breast-feeding.

Do not use Generic Parlodel in case of having uncontrolled high blood pressure, blood poisoning, having recently given birth or have coronary artery disease (chest pain) or any other severe heart disease.

In case you take Generic Parlodel while using birth control pills, remember that birth control pills become less effective

Patients under 15 years should be extremely careful with Generic Parlodel.

Avoid alcohol.

Be careful when you are driving machine.

It can be dangerous to stop Generic Parlodel taking suddenly.

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Studies investigating temperament traits in humans and their biological correlates have found high levels of novelty seeking (NS) linked with dopaminergic system changes, and particularly a deficit of dopamine transporter. Harm avoidance and reward dependence, on the other hand, appeared to be associated, respectively with serotonin and noradrenaline changes. In the present study, we have investigated the dopaminergic (DA), serotonergic (5-HT), and noradrenergic (NE) functions in healthy volunteers by challenging the monoamine systems with the DA agonist bromocriptine, the 5-HT agonist D-fenfluramine, and the NE agonist clonidine, respectively. Parallel to this investigation, we examined the temperament traits of our subjects by measuring NS, harm avoidance (HA) and reward dependence (RD) using the 'Three-dimensional Personality Questionnaire' (TPQ). The aims of the study were to see whether or not the monoamine functions were correlated with temperament traits. Bromocriptine challenge induced a significant GH increase and a significant suppression of PRL. D-fenfluramine test significantly increased PRL and cortisol plasma levels and Clonidine test induced a significant rise in GH values. NS scores showed a significant direct correlation with brom-stimulated GH values (r=0.426, P<0.05) and a significant inverse correlation with brom-inhibited PRL values (r=-0.498, P<0.01). HA scores correlated significantly with D-fen-stimulated PRL and CORT AUCs, (PRL: r=0.424, P<0.05; CORT: r=0. 595, P<0.005). RD scores correlated positively with clon-stimulated GH values (r=0.55; F=8.6; P<0.01) and negatively with brom-inhibited-PRL AUCs (r=-0.439, P<0.05). Our data support Cloninger theory concerning the biological correlates of temperamental traits, and evidence the link between the neuroendocrine responses to dynamic challenges and stable temperament features.

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Compared to the now numerous studies on the endocrinology of rheumatic diseases in adults, only a small number of studies has been published on children with rheumatic diseases. Prolactin has been most extensively investigated, showing interesting parallels with the findings in adults with rheumatological diseases. Thus, analogous to adult RA most forms of JRA or JCA (with the exception of ANA-positive JRA with uveitis) appear to show, if anything, low to normal levels of prolactin. Since the prolactin levels in adult RA depend on the inflammatory activity, and the physiological prolactin secretion decreases in chronic stress (especially sleep disorders), these results are most likely to be explained as reactive non-specific mechanisms in the stress of the disease. However, specific mechanisms are also being discussed to explain the low prolactin levels in adult RA. The results of prolactin measurements in juvenile SLE, juvenile ankylosing spondylitis and ANA-positive JRA with a raised incidence of uveitis, contrast with this. These conditions sometimes show significantly higher prolactin levels compared to healthy controls. A correlation of the increase of prolactin concentration with the inflammatory activity has been described for juvenile ankylosing spondylitis. These results correlate well with those of adult forms such as diseases of the seronegative spondyloarthropathies type, SLE and iridocyclitis. Raised prolactin concentrations are also found in these diseases. The inflammation promoting and immunostimulatory effects of prolactin found especially in animal experiments are confirmed clinically in these diseases by reports of successful treatments with the prolactin inhibitor, bromocriptine. The results available up to now for human growth hormone in JRA and JCA tend to be comparable with the results for prolactin in these form of paediatric rheumatological diseases. Besides normal values above, all lowered concentrations are measured for this hormone. Apart from other non-specific factors, its diminished secretion is mainly determined by the inflammatory activity of the disease. Low levels of growth hormone are likely to be a significant factor in the growth retardation in children with inflammatory rheumatological diseases. Up to now, the small number of investigations on gonadotrophins and the sex hormones in juvenile SLE and various forms of JRA published have not as yet yielded unequivocal results. The endocrine aspects of paediatric rheumatological diseases are thus still incompletely elucidated. However, there are many promising avenues for further fruitful research in this field.

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It is concluded that bromocriptine LAR is an effective treatment in the majority of patients with macroprolactinomas; it is also partially effective in some patients with GH secreting macroadenomas.

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The metabolic syndrome comprises a cluster of metabolic anomalies including insulin resistance, abdominal obesity, dyslipidemia, and hypertension. Previous studies suggest that impaired dopamine D2 receptor (D2R) signaling is involved in its pathogenesis. We studied the acute effects of bromocriptine (a D2R agonist) on energy metabolism in obese women; body weight and caloric intake remained constant. Eighteen healthy, obese women (BMI 33.2 +/- 0.6 kg/m(2), mean age 37.5 +/- 1.7, range 22-51 yr) were studied twice in the follicular phase of their menstrual cycle in a prospective, single-blind, crossover design. Subjects received both placebo (P; always first occasion) and bromocriptine (B; always second occasion) on separate occasions for 8 days. At each occasion blood glucose and insulin were assessed every 10 min for 24 h, and circadian plasma free fatty acid (FFA) and triglyceride (TG) levels were measured hourly. Fuel oxidation was determined by indirect calorimetry. Body weight and composition were not affected by the drug. Mean 24-h blood glucose (P < 0.01) and insulin (P < 0.01) were significantly reduced by bromocriptine, whereas mean 24 h FFA levels were increased (P < 0.01), suggesting that lipolysis was stimulated. Bromocriptine increased oxygen consumption (P = 0.03) and resting energy expenditure (by 50 kcal/day, P = 0.03). Systolic blood pressure was significantly reduced by bromocriptine. Thus these results imply that short-term bromocriptine treatment ameliorates various components of the metabolic syndrome while it shifts energy balance away from lipogenesis in obese humans.

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Anterior pituitary kallikrein-like enzyme activity, immunoreactivity and mRNA levels have previously been shown to be regulated by estrogen, in parallel with prolactin. In this study, we have examined the relationship between kallikrein and prolactin mRNA levels in estrogen-induced pituitary tumors. Treatment of Fischer 344 rats with diethylstilbestrol implants for 3, 5 and 7 weeks produced a dramatic increase in kallikrein mRNA levels and a modest increase in prolactin mRNA levels. These changes were partially reversed by bromocriptine treatment, and completely reversed by bromocriptine plus estrogen withdrawal. Using a panel of oligonucleotide probes specific for various members of the rat kallikrein gene family, we have shown that the kallikrein-like gene expressed appears to be true kallikrein.

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Mice were grouped to induce suppression of oestrus and subjected to removal of the vomeronasal organs or treatment with CB 154 which lowers prolactin levels. Both treatments overcame the suppression of oestrus after 72 h. Oestrus suppression was induced in lesioned mice by haloperidol treatment which raises plasma prolactin, and oestrus returned some 72 h after withdrawal of haloperidol treatment.

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Both PRL and GH play a role in maintaining lactation in the rat, although GH can only maintain pup weight gain at around 50% of the control value, whereas PRL can maintain weight gain close to 90% in the absence of GH. In this study we examined the effects of PRL and GH deficiency (using bromocriptine and an antiserum to rat GH) on milk yield and composition in lactating rats. Treatment with bromocriptine to suppress PRL secretion for 48 h led to a 57% decrease in milk yield with a concomitant decrease in milk protein and lactose yields, but no decrease in fat output. This led to the production of milk with a lower lactose concentration but increased concentrations of protein and particularly fat (increased 100%), which suggests that GH serves an auxiliary role by maintaining an energy-rich milk for the neonate when PRL secretion is reduced. This decrease in milk synthesis was accompanied by decreases in total mammary DNA content and increased milk sodium concentrations. The latter indicates the opening of tight junctions between mammary epithelial cells, which normally occurs during dedifferentiation and involution of the mammary gland. This suggests that PRL maintains milk synthesis at least in part by inhibiting epithelial cell loss and maintaining cellular differentiation. A deficiency in GH, by contrast, caused only a small decrease (24%) in milk yield and had no effect on the major constituents of milk or on milk sodium concentrations or total mammary DNA content. When animals were made deficient in both PRL and GH, however, there was a further marked decrease (88%) in milk volume along with the yields of all major milk constituents, confirming our previous findings that PRL and GH are the major regulators of milk synthesis. Recent studies have indicated that GH exerts direct effects on mammary gland growth, but its actions on milk secretion have been proposed to be mediated indirectly via insulin-like growth factor-I (IGF-I). We, therefore, inhibited lactation by inducing PRL and GH deficiency for 48 h and then attempted to reinitiate it by administering GH either systemically or by local oil-based implants into the mammary gland. Oil-based GH implants were as effective in stimulating milk secretion in the treated (but not contralateral, control) gland as was systemic GH treatment. Thus, GH does act directly on the mammary gland to stimulate milk synthesis, although this does not rule out the possibility that GH acts by stimulating local production of IGF-I.(ABSTRACT TRUNCATED AT 400 WORDS)

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The effect of the ergot derivative bromocriptine (5 mg orally) on blood pressure and plasma catecholamine concentrations was explored in normal volunteers. A significant decrease of plasma noradrenaline was found, while dopamine and adrenaline concentrations did not change significantly. Systolic and diastolic blood pressures were significantly lowered at 150 min after administration. The hypotensive effect of bromocriptine seems to be mediated by a lowered release of noradrenaline from sympathetic nerve endings. It may be hypothesized that the drug stimulates presynaptic dopamine receptors located on postganglionic sympathetic nerves, thus inhibiting noradrenaline discharge.

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Results from five experiments are reported. Male dwarf hamsters (Phodopus spp.) were housed in modified home cages under continuous flow of compressed air that could be switched to isoflurane in O2 vehicle without approaching the cages.

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Clozapine is an atypical neuroleptic drug that was initially thought not to cause neuroleptic malignant syndrome (NMS). We report a case of NMS associated with clozapine as a single agent that developed in a patient with no prior history of NMS. In contrast to other reported cases of NMS with clozapine monotherapy in which rigidity was reported to be absent, our patient had classic NMS with lead-pipe rigidity. NMS should be included in the differential diagnosis of a febrile patient with a history of any neuroleptic treatment, including clozapine.

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Rats were trained to discriminate the putatively selective dopamine (DA) receptor agonists SKF 38393 (10 mg/kg) or Ly 171555 (0.025 mg/kg) from saline in a two-lever situation involving fixed-ratio (FR 20), extinction schedules of water reinforcement. During substitution tests, no dose of any compound [apomorphine, Ly 171555, lisuride, LSD, amphetamine, cocaine, (-) 3-PPP, or SKF 82526] mimicked SKF 38393, the effects of which were blocked by the D1 antagonist Sch 23390 but not by haloperidol. Postsynaptic and DA "autoreceptor" agonists [apomorphine, (-) 3-PPP], as well as dopaminergic ergot derivatives (bromocriptine, lergotrile, lisuride) and Sch 23390, substituted for Ly 171555, a partial ergoline which has behavioral effects that are blocked by haloperidol and molindone, but not by either Sch 23390 or serotonin (5-HT) antagonists (ketanserin, pizotifen). Amphetamine and cocaine did not substitute for either SKF 38393 or Ly 171555. These results suggest that the stimulus properties of a variety of neuropharmacologically important and clinically useful compounds are transduced at (pre- or postsynaptic) D2 receptors. However, this conclusion must be tempered by evidence that actions at D1 and D2 receptors may not be entirely independent. The behavioral effects of abused psychomotor stimulants probably involve mechanisms other than "direct" agonist activity at either D1 or D2 receptors.

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A recent psychobiological theory postulates a dopaminergic basis for the agency facet of extraversion, leading to the prediction that this personality trait modulates the psychophysiological effects of dopaminergic drugs. A single dose of the dopamine D2 receptor agonist bromocriptine reduces blood pressure in healthy volunteers. However, it is currently unknown whether this hypotensive effect of bromocriptine is modulated by agentic extraversion. Therefore, we measured resting cardiovascular activation in groups of healthy male volunteers either high or low in agentic extraversion, either under bromocriptine (1.25 mg) or placebo. Focusing the analyses on activation components derived from 18 cardiovascular variables, we found that bromocriptine reduces alpha-adrenergic activation in the sample as a whole, whereas the effects on beta-adrenergic and cholinergic activation are modulated by agentic extraversion.

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Bromocriptin, member of the class of ergolines, is commonly prescribed as treatment of Parkinson's disease. Apart from vascular, digestif, neurologic and psychic disorders, the authors report cases of retroperitoneal fibrosis and pleural effusion, as adverse reactions related to the bromocriptin.

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This prospective study includes 31 women with a prolactin (PRL) level greater than 20 ng/ml (upper limits of normal in our laboratory) on at least three different occasions and chemically euthyroid. Each woman received bromocriptine mesylate (BRC) 1.25 mg (1/2 tablet)/day for 2 weeks, at which time a repeat PRL level was obtained. If needed, the dose was increased in a stepwise fashion until the PRL level was in the normal range. Results show that 12 of 15 patients with an initial PRL greater than 20 but less than 50 ng/ml required 2.5 mg or less of BRC daily. Of 9 patients with a PRL greater than 50 but less than 100 ng/ml, 5 required 2.5 mg daily with the remaining 4 needing 5.0 mg. Five of 7 patients with a PRL greater than 100 ng/ml required 5.0 mg or more, while one responded to 1.25 mg. These findings confirm that a lower than manufacturer-recommended dose of BRC is usually effective in normalizing PRL levels, especially when the initial PRL is less than 100 ng/ml.

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The basal levels of prolactin (PRL) and their changes after i.v. thyrotropin releasing hormone (TRH) administration after bromocriptine (BCT) pretreatment (BCT/TRH test) were monitored in 12 patients with young-onset Parkinson's disease (PD) (before 40 years of age) and 10 patients with older-onset PD (after 40 years of age), as well as in two groups of healthy subjects (10 persons in each), age-matched with older-onset (control A) and young-onset (control B) parkinsonians. The basal PRL levels were normal in both groups of patients. When given after BCT, TRH induced a significantly lower PRL increase in older-onset parkinsonians than in controls. This response was even more blunted in young-onset patients, being significantly more attenuated than in older-onset PD patients.

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Patients receiving stable doses of MTX were randomized to one of two groups and received 3 months of double-blind bromocriptine (5 mg/day) or matching placebo. The moderate and major outcome measures were the proportion of patients with > 0.6 and > 1.2 improvement in RA based on the Disease Activity Score 28 (DAS28) at 3 months. Safety measures included adverse events and laboratory assessments.

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The 220 suspected AEs fell into five categories: (i) syncopal/pre-syncopal, (ii) fibrotic, (iii) psychotic, (iv) obsessive-compulsive behaviours (OCB) and (v) increased sleep. There were differential lag times between initial individual drug registration and reporting of suspected AEs, with a lag of at least one year for fibrotic reactions and OCB compared to more contemporaneous reporting of other AEs. Consistent with the published literature, ACSOM data showed that ergot DAs share fibrotic reactions as a class AE, whereas symptomatic hypotensive reactions, psychosis and OCB occurred in both ergot and non-ergot DAs, cabergoline and pramipexole, respectively. Reports of syncopal and pre-syncopal reactions seemed to diminish as ergot-based DA use declined. Levodopa was taken simultaneously with DAs in 87 instances. Of those treated, 92 % were 50 years or older. Parkinson's disease accounted for 89 % of use (119 reports).

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Ovulatory volunteers were randomized to receive either oral or vaginal bromocriptine (2.5 mg). In a second session, the subjects were crossed-over to bromocriptine by the alternate route. An additional hyperprolactinemic patient received vaginal bromocriptine only.

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In the course of a clinical trial with 2alpha-bromoergocryptin in Parkinson's disease, the serum levels of several pituitary hormones have been studied in the assumption that the drug active on nigro-striatal dopaminergic system might also interfere with hypothalamus-protuberantial neurotransmission, and have effects on the function of the pituitary. No changes in serum levels of FSH, LH, STH and TSH were detected for every dose of the drug employed. Only prolactin serum levels diminished since the beginning of the treatment, the decrease being significant (p less than 0.05 and p less than 0.01). This effect on prolactin does not change in the dose range considered. Clinical improvement was observed for doses of drugs above 15 mg/day, whereas the effect on prolactin secretion occurred with the dose of 7.5 mg/day.

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Semantic priming is a function related to prefrontal cortical (PFC) networks and is lateralized. There is evidence that semantic priming underlies dopaminergic modulation. It is known that the D1-receptor is more abundant in prefrontal networks; however, until now there have been no studies investigating the selective modulation of semantic priming with dopamine agonists. Furthermore, D1 receptor dysfunction has been described in schizophrenia, and patients with formal thought disorder seem to have disturbed focusing of associations and increased indirect priming.

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Impairment of language function (aphasia) is one of the most common neurological symptoms after stroke. Approximately one in every three patients who have an acute stroke will suffer from aphasia. The estimated incidence and prevalence of stroke in Western Europe is 140 and 800 per 100,000 of the population. Aphasia often results in significant disability and handicap. It is a major obstacle for patients to live independently in the community. When recovery from aphasia occurs, it is usually incomplete and patients are rarely able to return to full employment and other social activities. Currently, the main treatment for aphasia is conventional speech and language therapy. However, the effectiveness of this intervention has not been conclusively demonstrated and empirical observations suggest that spontaneous biological recovery may explain most of the improvement in language function that occurs in aphasics. The generally poor prognosis of the severe forms of poststroke language impairment (Broca, Wernicke and global aphasia), coupled with the limited effectiveness of conventional speech and language therapy has stimulated the search for other treatments that may be used in conjunction with speech and language therapy, including the use of various drugs. Dopamine agonists, piracetam (Nootropil), amphetamines, and more recently donepezil (Aricept), have been used in the treatment of aphasia in both the acute and chronic phase. The justification for the use of drugs in the treatment of aphasia is based on two types of evidence. Some drugs, such as dextroamphetamine (Dexedrine), improve attention span and enhance learning and memory. Learning is an essential mechanism for the acquisition of new motor and cognitive skills, and hence, for recovery from aphasia. Second, laboratory and clinical data suggest that drug treatment may partially restore the metabolic function in the ischemic zone that surrounds the brain lesion and also has a neuroprotective effect following acute brain damage. An example of this is the nootropic agent piracetam. Extensive animal studies have demonstrated the beneficial effects of this and other drugs on neural plasticity, but data on humans are still sparse. This review provides a critical analysis of the current evidence of the effectiveness of these drugs in the treatment of acute and chronic aphasia.

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Specific features in the course of pregnancy and labor were studied in 24 hyperprolactinemic women after parlodel stimulation. A high incidence of threatened abortions (7 cases), late gestosis (7 cases), fetal hypoxia (5 cases), early rupture of amniotic fluid sac (4 cases), surgical delivery (3 cases) was noted. Regular clinical and biochemical check-ups are necessary during pregnancy and postpartum. The data permit a conclusion that women in whom pregnancy resulted from parlodel stimulation should be referred to a risk group.

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The effects of a GnRH antagonist analogue (N-acetyl-Ala1,D-p-Cl-Phe2,D-Trp3,6-GnRH, Ant.) and a GnRH antiserum (A/S) on the development of pituitary-testicular function were studied in immature (23/24-31/32-day-old) rats. In another experiment the Ant. treatment was combined with bromocriptine (BR)-induced hypoprolactinaemia. Ant. and A/S decreased serum and pituitary levels of LH and FSH, and BR those of Prl (P less than 0.01-0.05). Testicular testosterone (T) and progesterone (P) contents were significantly decreased only by Ant. (P less than 0.01). Ant. decreased the weights of the testes, ventral prostates and seminal vesicles, as well as testicular LH, FSH and Prl receptors (R) (P less than 0.01-0.05). BR decreased LH-R but had no effect on Prl-R. Both Ant. and A/S decreased available pituitary GnRH-R (P less than 0.01), but free testicular GnRH-R were reduced only by Ant. BR increased GnRH receptors in the pituitaries. It is concluded that Ant.-induced low gonadotropin levels in immature animals inhibit the developmental increase of testicular weight, gonadotropin and Prl-R, steroidogenesis and androgen action on accessory sex glands. Hypoprolactinaemia had an additive inhibitory effect to the antigonadal effects of Ant. The testis tissue of immature (23/24-day-old) animals already contains GnRH-R. In general, developing animals are clearly very sensitive to the antigonadal actions of Ant. and BR, whereas the effect of GnRH-A/S is less pronounced than in adults.

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The production of testosterone (T) by decapsulated mouse testes in vitro was significantly stimulated by 2-Br-alpha-ergocriptine (bromocriptine) at concentrations ranging from 1 ng/ml to 5 microgram/ml. In the presence of a low dose of human chorionic gonadotropin (hCG), bromocriptine produced a further increase in T production, whereas in the presence of a high concentration of hCG it was ineffective. It is suggested that a direct stimulatory effect of bromocriptine on testicular steroidogenesis may contribute to its therapeutic effects in hyperprolactinemic men.

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In a group of 16 females and 2 males with hypogonadism and hyperprolactinemia, bromocriptine was found to suppress prolactin (PRL) high levels within one day without further significant lowering during a 3 weeks longitudinal survey. The usually effective dosage was 5 mg per day. On the contrary, sex hormones did not vary initially and increased secondarily only in those patients resuming gonadal activity. The changes were either cyclical or heterogenous when the first cycle was anovulatory. This latter situation could sometimes but not always be attributed to persistent hyperprolactinemia. Menstruation resumed in 11 patients. Persistance of hypogonadism in the remainder could be explained by incomplete PRL reduction in one case and probability of previous hypothalamo-pituitary damage in six. The latter hypothesis was based in part on impaired gonadotropins responses to LH RH which were not modified by the treatment.

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We have established that estradiol accelerates apoptosis in the CL during post-partum luteal regression through a mechanism that possibly involves the secretion of pituitary prolactin. We have also shown that the post-partum rat CL express ERalpha and ERbeta mRNAs suggesting that they can be targeted by estrogen.

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Resting growth hormone and prolactin levels and dynamic responses to bromocriptine and metoclopramide have been measured in epileptic patients before treatment, and compared with a matched group taking phenytoin alone. Mean resting levels of prolactin were higher in patients taking phenytoin (untreated patients 204 mU/l, phenytoin treated patients 302 mU/l), but dynamic responses to metoclopramide and bromocriptine were unaffected. Mean resting levels of growth hormone were also higher in patients taking phenytoin (untreated patients 1.4 mU/l, phenytoin treated patients 6.0 mU/l) and paradoxical suppression was seen following bromocriptine. Phenytoin is unlikely to have any major action on the D2 receptor present on the lactotroph. The abnormalities in growth hormone may explain the well recognized effects of phenytoin on connective tissue.

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Twenty-three patients with active acromegaly underwent serum sampling for growth hormone (GH), insulin and insulin-like growth factor binding protein 1 (IGFBP-1) after placebo or single doses of octreotide or bromocriptine. Integrated 24-h serum GH levels decreased by 90% after octreotide and 49% after bromocriptine. A statistically significant correlation between the course of GH levels after octreotide and bromocriptine was observed (p < 0.001). Octreotide, but not bromocriptine, induced a significant increase in integrated 24-h serum IGFBP-1 levels to 37.4 times the baseline values. Bromocriptine caused a non-significant increase in integrated 24-h serum IGFBP-1 levels, which argues against a direct regulatory effect of GH on IGFBP-1 production in acromegaly. In conclusion, octreotide induces in acromegaly the production of IGFBP-1, which occurs independently of the number of somatostatin receptors on the GH-secreting pituitary adenoma. The supposed inhibitory effect of IGFBP-1 on the biological effect of IGF-1 might result in an additional clinical benefit in acromegalic patients as compared to treatment directed at the pituitary level.

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1. The oral administration of 2.5 mg of the dopamine (3,4-dihydroxyphenethylamine) agonist bromoergocriptine enhanced the osmotically stimulated rise in plasma [arginine]vasopressin ([Arg]VP) concentrations in five normal human subjects. 2. This finding lends support to the suggestion that the osmotically induced release of [Arg]VP is under dopaminergic control in man.

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The surgical treatment of prolactinomas protects against the complications that these tumours have, but by itself does not cure the infertility which is found in at most 50% of all cases. The value of radiotherapy is limited to those cases where there is a contra-indication for carrying out surgery and in the tumours that have been incompletely removed and when pregnancy is not desired. The principal drugs used to lower prolactin are the dopamine agonist, which is bromocriptine and the serotonin antagonist which is methergoline which is less powerful than bromocriptine. Bromocriptine brings about normal prolactinaemia and ovulation is re-established and menstruation returns in most cases of idiopathic hyperprolactinaemia and in many cases where hyperprolactinaemia is due to a tumour. It, in certain cases, has an antitumoral effect and can definitely cure some hyperprolactinaemias whether they are tumoral or not. So bromocriptine is the specific treatment of women whose sterility is due to hyperprolactinaemia and no teratogenic effect has been reported. The only complications that have occurred in pregnancies that have been induced by this drug have been growths in the tumours in women who have pituitary adenomata, but these complications are far less frequent and serious in cases of micro-adenomata. Since the antitumoral effect of bromocriptine has been discovered the indications for surgery have lessened but it is often all the same necessary. The medical treatment of adenomata can only be considered when strict supervision is going to be undertaken. Bromocriptine can also establish ovulation in a few categories where ovulation occurs in normoprolactinaemic women and it can also be used as a treatment for the premenstrual syndrome.

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Biphasic effects of bromocriptine (2.0, 5.0, 10.0, and 20.0 mg/kg IP) on locomotion were quantified in photocell activity boxes in rats. Following early suppression of activity, bromocriptine produced a clear, dose-dependent increase in locomotion that lasted several hours. When a low dose of bromocriptine (5.0 mg/kg) was administered daily over a 3-week period, the locomotor-activating effects of the drug showed progressive enhancement over days. The sensitization was environment specific; rats administered bromocriptine six times in the home cage showed no sign of a sensitized response to bromocriptine when subsequently tested in the activity box. Thus, selective stimulation of D2 receptors stimulates locomotion and sensitizes animals to subsequent injections, just as do the indirect-acting dopamine agonists cocaine and amphetamine.

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Neuroleptic malignant syndrome is a relatively uncommon life-threatening disorder. The widespread use of the neuroleptic and psychotropic medications, however, makes it important for the primary care physician to understand the clinical presentation, differential diagnosis, and management of neuroleptic malignant syndrome. Early recognition should be possible. Rapid diagnosis followed by aggressive supportive care and specific pharmacologic therapy can be life saving.

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The effect of bromocriptine on acetylcholine (ACh) output from the cerebral cortex was investigated in anaesthetized rats. Bromocriptine caused a brief decrease in ACh output at the dose of 0.1 mg/kg i.p. and a dose-related long-lasting increase at doses from 1.25 to 10 mg/kg i.p. Apomorphine elicited an increase in ACh output when injected intraperitoneally at doses from 0.1 to 10 mg/kg. When bromocriptine was administered to rats in which a septal lesion had been made 12 days prior to the test, no increase in ACh output was observed. Bromocriptine seems therefore to stimulate a cortical cholinergic pathway originating from or passing through the septum.

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To elucidate the neurochemical mechanism that underlies the effect of anti-parkinsonian agents on motor activities in the dopamine-depleted striatum, we evaluated AP-I and CREB DNA-binding activity in the striatum of 6-hydroxydopamine-lesioned rats by use of a gel mobility-shift assay. Rats with a unilateral lesion of the nigrostriatal dopamine pathway were injected i.p. with either SKF38393 (a DI receptor agonist), bromocriptine (a D2 receptor agonist), or levodopa (a Dl/D2 receptor agonist). Each treatment increased the number of rotational responses of rats contralateral to the lesioned side. However, only SKF38393 and levodopa increased AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. As with the expression of c-fos, supersensitive DI receptors may play a key role in the enhanced induction of AP-I and CREB DNA-binding activity in the dopamine-depleted striatum. Supershift analysis revealed that c-Fos; and Jun family proteins are the main components for AP-1 induced in the dopamine-depleted striaturn by SKF38393 or levodopa.

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The mechanism and hormonal regulation of lactation is explained and illustrated with a schematic representation. Circulating estrogen above a critical amount seems to be the inhibitory factor controlling lactation during pregnancy. Once delivery occurs, the level of estrogen falls, that of prolactin rises, and lactation begins. Nonsuckling can be used to inhibit lactation. Estrogens can also be used to inhibit lactation more quickly and with less pain. The reported association between estrogens and puerperal thromboembolism cannot be considered conclusive due to defects in the reporting studies. There is no reason not to use estrogens in lactation inhibition except for women over 35 who experienced a surgical delivery. Alternative therapy is available for these women. The recently-developed drug, brom-ergocryptine, may replace other methods of lactation inhibition.

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parlodel buy 2017-08-05

Bromocriptine produces long-lasting hypomotility and decreases brain dihydroxyphenylacetic acid (DOPAC) in mice. These effects are obtained with doses much lower than those which produce hypermotility. The decrease of brain DOPAC is correlated to the hypomotility both on a dose and on a time basis. Potent DA receptor blockers as pimozide, benzperidol and droperidol antagonize the hypomotility and the decrease of brain DOPAC produced by bromocriptine. These effects are obtained with very low doses (0.05-0.3 mg/kg) of neuroleptics which per se do not affect motility or brain DOPAC. The maximal decrease of brain DOPAC produced by bromocriptine is similar to that produced by apomorphine and the combination of these drugs does not result in a further decrease. On the basis of these results it is postulated that bromocriptine decreases DA turnover and produces hypomotility by acting on "regulatory" parlodel buy DA receptors different from the postsynaptic ones of the "terminal" dopaminergic areas.

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It is difficult to achieve pregnancy in hyperprolactinaemic patients in whom prolactin inhibiting agents are ineffective. Medical treatment with bromocriptine, lisuride and the new agent CV 205-502 (quinagolide parlodel buy ) was unsuccessful in normalizing hyperprolactinaemia in a 28 year-old woman to treat anovulatory infertility. Repeated Magnetic Resonance Imaging (MRI) was normal, with no images suggestive of prolactin adenoma. A live child was born after pulsatile GnRH treatment despite persistently elevated prolactin levels; normal MRI and decreased prolactin levels were observed after pregnancy. In summary, successful pregnancy can be obtained with pulsatile GnRH treatment in women resistant to old and new medical treatments of hyperprolactinaemia.

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Randomised and controlled clinical trials comparing dopamine agonists alone or associated with Benicar Dosage Range psychosocial intervention with placebo, no treatment, other pharmacological interventions

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34 crossbred and purebred Trental Pentoxifylline Tablets bitches referred for possible pregnancy termination. Seven additional pregnant bitches were used as controls.

parlodel buy 2016-08-09

30 women (35-54 yrs) were treated with fine Zofran Mg needle aspiration and afterwards with bromocriptine, estrogen-progestogens and progestogens.

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In the treatment group bromocriptine was given intramuscularly to 22 patients after their first kidney transplantation along with conventional immunosuppression (cyclosporin A, glucocorticoids). Twenty-three Trental Drug Category patients receiving only conventional immunosuppression served as control subjects. The incidence of acute graft rejections, graft losses, and infections was evaluated.

parlodel buy 2017-03-21

Human hepatocarcinoma cell line HepG(2) (HepG(2) group), drug resistant hepatocarcinoma cell line HepG(2)/adriamycin (HepG(2)/ADM group) and hepatocarcinoma cell line transfected with TNF-alpha gene HepG(2)/ADM/TNF (TNF group and BCT group) were injected into the liver of nude mice via orthotopic implantation to establish multidrug resistance model of liver neoplasm in vivo. All the mice were injected with 5-fluouracil + adriamycin + mitomycin in abdominal Motilium Liquid Dosage cavity for 7 d. The mice in BCT group was simultaneously given bromocriptine through gastric canal. Size and weight of the tumor were measured. Furthermore tumor histological character and growth of the nude mice was observed and its chemosensitivity was tested. MDR associated genes and proteins (MRP, LRP) of implanted tumors were detected by immunohistochemical staining and reverse transcriptive polymerase chain reaction (RT-PCR), and apoptosis rate of hepatocarcinoma cells was detected by TUNEL assay.

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These results support Glucovance 500 Mg the hypothesis that dopaminergic mechanisms mediate cigarette smoking reinforcement.

parlodel buy 2016-06-15

Pituitary apoplexy is a rare and life-threatening clinical condition caused by hemorrhage and/or infarction of the pituitary gland or adenoma. Although pituitary apoplexy is usually spontaneous, it has been associated with numerous precipitating factors, such as bromocriptine use. However, reports of pituitary apoplexy Myambutol Drug during cabergoline therapy are scarce. We report three patients with cystic macroprolactinomas who developed pituitary apoplexy during cabergoline treatment.

buy parlodel online 2016-11-07

a) describe the relationship between hyperprolactinemia and fertility, b) review the results of the use of dopamine Albenza 400mg Cost agonists during pregnancy and embryo-fetal development and c) review the therapeutic management in micro and macroprolactinomas during pregnancy.

parlodel buy 2017-08-21

The percentage of successful pregnancies was higher in the bromocriptine-treated group than in the group that was not treated with bromocriptine (85.7% versus 52.4%, P < .05). Serum prolactin levels during Famvir Tablet early pregnancy (5-10 weeks of gestation) were significantly higher in patients who miscarried (31.8-55.3 ng/mL) than in patients whose pregnancies were successful (4.6-15.5 ng/mL, P < .01 or P < .05).

buy parlodel online 2016-08-28

New concepts about the pathogenesis and pathophysiology of Parkinson's disease have emerged. For these concepts to be useful, they must be understood, and for them to be applied, the psychology of the patient and the patient's family must be understood. The initial consultation is crucial in establishing a successful relationship between a patient, family, and physician. This consultation is analyzed Prograf Capsules and ways of avoiding errors and misconceptions delineated. Emphasis is placed on imaginitive questioning using the format of the ADL portion of the UPDRS in establishing the diagnosis and following treatment. The rational for starting treatment with selegiline at this time is discussed in the context of the role that increased MAO-B activity plays in the progression of Parkinson's disease. After making the diagnosis and starting treatment with selegiline, deciding when to start levodopa is the next crucial decision. Often as important as deciding when to start levodopa is overcoming the resistance of the patient to accept this treatment. The next crucial decision occurs after the patient develops response fluctuations on levodopa. A format for assessing the fluctuations is presented, and the merits of different treatments, including selegiline, dopamine agonists (bromocriptine and pergolide), and sustained-release or controlled-release levodopa preparations (Sinemet CR), discussed. The management of patients with depression, sleep problems, and advanced disease including postural instability and mental changes are reviewed.

parlodel buy 2017-02-12

Sixteen new compounds 2-methylamino substituted phenyl-3-substituted anilino 4 (3H) quinazolinones (3-18) were prepared. All the compounds were evaluated for their antiparkinsonian activity Imitrex Injection Reviews and compared with bromocriptine. Compounds 10,15 and 18 showed better activity. These compounds also bind with the dopamine receptors in striatal membrane preparations of rat brain.

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We previously reported a reduction of glucocorticoid receptors (GCR) in diethylstilbestrol-induced pituitary tumors (DES-T) in rats. Presently, we found that bromocriptine (BROM) treatment increased the levels of GCR in DES-T, demonstrated by steroid binding assays and immunocytochemistry using a monoclonal antibody against the type II GCR. We also found that the high content of nuclear estradiol receptors in the adenomata and the elevated levels of PRL in serum of DES-T were significantly reduced after BROM treatment. In parallel studies, PRL secretion was measured after administration of ether stress. In controls, serum PRL markedly increased after ether and this effect was blunted by prior dexamethasone (DEX) administration, due to the steroid negative feedback on PRL secretion. In animals with DES-T, ether stress had no effect on serum PRL, and the inhibition by DEX was lost unless they received BROM, which restored the negative feedback of DEX on serum PRL. Although increases of PRL titers in pituitary tumors may be due to estrogenic stimulation of lactotroph proliferation and function, coupled to absent dopaminergic inhibition on these cells, other mechanisms are possible. In this respect, inefficient steroid negative feedback on PRL synthesis due to down-regulation of GCR may contribute to hyperprolactinemia. This mechanism is supported from the restoration of GCR and steroid negative feedback on serum PRL by treatment of tumor-bearing rats with BROM.

parlodel buy 2016-03-02

In this systematic review we present information relating to the effectiveness and safety of the following interventions: antibiotics, bromocriptine, combined oral contraceptive pill, danazol, diuretics, evening primrose oil, gestrinone, gonadorelin analogues, hormone replacement therapy (HRT), lisuride, low-fat diet, progestogens, pyridoxine, tamoxifen, tibolone, topical or oral non-steroidal anti-inflammatory drugs (NSAIDs), toremifene, and vitamin E.

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Patients with prolactinoma are commonly treated with the D2 dopamine agonist bromocriptine, which in most cases, normalizes prolactin (PRL) levels. However, resistance to bromocriptine has been observed in 5 to 18% of tested prolactinomas and is associated to a decrease in both D2 receptor density and mRNA levels. In this study, we used quantitative RT-PCR to investigate whether expression of G alpha proteins could be also modified in bromocriptine resistant prolactinomas. No difference in G alpha o mRNA levels or in the relative expression of G alpha s between bromocriptine sensitive and bromocriptine resistant prolactinomas was observed. In contrast, the relative expression of G alpha i2 was found to be decreased in bromocriptine resistant prolactinomas when compared to that of bromocriptine sensitive prolactinomas. Interestingly, the relative G alpha i2 expression was correlated to both bromocriptine inhibition of in vitro PRL secretion and D2 receptor mRNA levels. Bromocriptine resistance could thus result from a decrease in D2 dopamine receptors associated with a decrease in G alpha i2 expression.

parlodel buy 2016-12-11

The pharmacological characteristics and the microanatomical localization of dopamine D(2)-like receptors, or more correctly spiroperidol binding sites, in the rabbit pulmonary circulation were studied using combined marker binding and light microscopy autoradiography with [((3))H]-spiroperidol (spiperone) as marker. The marker was bound to the samples of the pulmonary artery in a manner consistent with the labelling of dopamine D(2)-like receptors with an equilibrium dissociation constant (K(d)) of about 2.4+/-0.07 nmol/l and a maximum density of binding sites of 65+/-4.5 fmol/mg tissue. Samples of bronchial artery show the same results as those of the pulmonary artery. In contrast, binding experiments made with samples of rabbit lung (capillary of the microcirculation), of pulmonary veins and/or of bronchial veins did not allow the evaluation of specific binding.Autoradiography, observed with light microscopy, showed the development of specific silver grains within the whole wall of extraparenchymal branches of the pulmonary artery and/or of the bronchial artery. Development of silver grains was inhibited by compounds active on the dopamine receptors. The greater sensitivity to displacement by domperidone, haloperidol, and bromocriptine than to displacement by N-propyl-nor-apomorphine, quinpirole and clozapine suggests that the binding sites observed in extraparenchymal, large and medium-sized branches of the rabbit pulmonary and bronchial arteries belong, likely, to the dopamine D(2) receptor subtype. Quantitative analysis of images let us count the amount of these receptors in many samples of the pulmonary and/or bronchial arteries.

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To investigate the site and mode of action of progesterone in inducing gonadotropin release, the effects of catecholamine-depleting (methyldopa) or dopamine agonist (bromocriptine) drugs on progesterone positive feedback and the gonadotropin response to a centrally acting noradrenergic drug (clonidine) were evaluated in estrogen-primed postmenopausal women. Progesterone administration induced a significant rise in LH, FSH, and PRL serum levels in the control group. Bromocriptine administration was followed by a marked suppression of PRL release but did not modify the gonadotropin response to progesterone. Methyldopa pretreatment significantly reduced the progesterone-induced LH surge, while PRL release was unaffected. After estrogen priming, clonidine administration did not result in an increase in serum LH or FSH concentrations. The dissociated responses of LH and PRL in bromocriptine-pretreated subjects and the significant reduction of the LH rise after progesterone in methyldopa-pretreated women seem to invalidate the hypothesis that a fall in endogenous dopamine is responsible for progesterone positive feedback and suggest that neural noradrenergic mechanisms are involved in progesterone-induced gonadotropin release. The ineffectiveness of a centrally acting noradrenergic agonist in inducing gonadotropin rise provides indirect evidence that an increased pituitary responsiveness may also be involved in progesterone positive feedback.

parlodel buy 2017-01-17

In the rat, the maintenance of gestation is dependent on progesterone production from the corpora lutea (CL), which are under the control of pituitary, decidual and placental hormones. The luteal metabolism of progesterone during gestation has been amply studied. However, the regulation of progesterone synthesis and degradation during pseudopregnancy (PSP), in which the CL are mainly under the control of pituitary prolactin (PRL), is not well known. The objectives of this investigation were: i) to study the luteal metabolism of progesterone during PSP by measuring the activities of the enzymes 3beta-hydroxysteroid dehydrogenase (3betaHSD), involved in progesterone biosynthesis, and that of 20alpha-hydroxysteroid dehydrogenase (20alphaHSD), involved in progesterone catabolism; and ii) to determine the role of decidualization on progesterone metabolism in PSP.

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A case of NMS was reported. NMS is an uncommon but potentially lethal complication of treatment with neuroleptics. The diagnosis of NMS should seriously be considered in any individual receiving neuroleptic medications who develops unexplained fever associated with muscle rigidity. The discontinuation of neuroleptics and the use of general supportive measures are crucial. On the basis of more rapid clinical response, either bromocriptine or dantrolene could be added to traditional supportive care.

parlodel buy 2017-09-06

Rats were trained to discriminate the cue produced by 0.25 mg/kg apomorphine from that produced by saline, using a two-lever, drug discrimination task. This cue was blocked by haloperidol but not by DPI, ergometrine, bromocriptine, sulpiride, naloxone or naltrexone; none of these agents substituted for (mimicked) apomorphine. Morphine and levorphanol did, however, mimic apomorphine, whereas dextrorphan did not; pentazocine induced responding unlike either apomorphine or saline. The substitution of morphine for apomorphine was blocked by naltrexone or bromocriptone, and was partially antagonized by a low of ergometrine, but was unaffected by haloperidol or sulpiride. To explain these results, it was proposed that morphine mimics apomorphine by inhibiting dopaminergic autoregulation involving D2-receptors.

buy parlodel online 2017-06-09

It is well established that TRH exerts a stimulatory effect on the secretion of both TSH and PRL. Clinically, hyperprolactinemia is usually present in hypothyroid women, but not men. In experimental studies, results vary because of the sexes, and treatments of animals differ. The purpose of this study was to further investigate the physiological control of PRL secretion in hypothyroid female rats. Adult female Sprague-Dawley rats that were surgically ovariectomized (OVX) and/or thyroidectomized (Tx) for 2 weeks were used. Serial blood samples were collected through indwelling intraatrial catheters, and plasma PRL and TSH levels were measured by RIA. We found that OVX + Tx and polyestradiol phosphate (PEP; 0.1 mg/rat, sc)-treated rats exhibited significantly higher basal PRL and TSH levels and afternoon surge PRL levels than sham Tx rats with the same treatments. On the other hand, if OVX + Tx rats were not treated with estrogen, their plasma PRL levels were not significantly different from those in sham Tx controls. If challenged with TRH (1 microgram/rat, iv), significantly higher PRL responses were found in OVX + Tx + PEP rats than in sham Tx rats. The contents of TRH in the median eminence of Tx rats, however, were not different from those in sham Tx rats. When challenged with domperidone (10 micrograms/rat, iv), a dopamine antagonist, no difference in PRL increments was found in the two groups of animals. Treatment with CB154, a potent dopamine agonist, did not eliminate the difference in basal PRL levels between the two groups. Pretreatment with a smaller dose of domperidone (1 microgram/rat), however, enhanced the PRL-releasing effect of TRH more in Tx than in sham Tx rats. When T4 (2 or 10 micrograms/100 g BW.day for 21 days) was replaced in Tx rats starting the second day after Tx, both basal and TRH-stimulated PRL secretion were significantly decreased in a dose-dependent manner. In conclusion, the increased PRL levels in OVX + Tx + PEP rats may be due to increased responsiveness of the anterior pituitary gland to TRH, and not to a decreased responsiveness to dopamine. In addition, the elevation of plasma PRL in OVX + Tx + PEP rats is negatively correlated with plasma levels of thyroid hormone.

parlodel buy 2017-11-10

Seasonally obese hyperinsulinemic hamsters were treated for 5 weeks with bromocriptine (500 to 600 micrograms per animal) and tested for drug effects on energy balance, body fat stores, nocturnal whole-body free fatty acid (FFA) metabolism and hepatic glucose output, and diurnal glucose tolerance. After 5 weeks, bromocriptine treatment reduced retroperitoneal fat pad weight by 45% without altering either daily food consumption or end-treatment total daily energy expenditure. Also, 5 weeks of treatment improved the diurnal glucose tolerance, resulting in a 47% and 33% decrease in the area under glucose and insulin curves, respectively. After 4 weeks, bromocriptine treatment reduced nocturnal lipolysis by 28%, palmitate rate of appearance into plasma by 30%, palmitate oxidation by 33%, and hepatic glucose output by 28%. Moreover, these reductions were accompanied by a 75% reduction in plasma insulin concentration. The data suggest that bromocriptine may improve diurnal glucose tolerance in part by inhibiting the preceding nocturnal lipolysis and FFA oxidation. Reductions in nocturnal FFA oxidation and hepatic glucose production may result from bromocriptine's influences on circadian organization of hypothalamic centers known to regulate these activities. Available evidence suggests that bromocriptine may impact this neuroendocrine organization of metabolism by increasing the dopamine to noradrenaline activity ratio in central (hypothalamic) and peripheral (eg, liver and adipose) target tissues.