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Motilium

Generic Motilium is a medicine that increases the movements or contractions of the stomach and bowel. Generic Motilium is also used to treat nausea and vomiting caused by other drugs used to treat Parkinson's Disease.

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Description

Generic Motilium is a medicine that increases the movements or contractions of the stomach and bowel. Generic Motilium is also used to treat nausea and vomiting caused by other drugs used to treat Parkinson's Disease.

Generic Motilium works by blocking the action of a chemical messenger in the brain which causes the feeling of nausea and vomiting, as well as increasing the movement or contractions of the stomach and intestines, allowing food to move more easily through the stomach.

Motilium is also known as Domperidone, Dombax, Vivadone, Motinorm, Costi.

Generic name of Generic Motilium is Domperidone.

Brand name of Generic Motilium is Motilium.

Dosage

The usual dose in adults is one tablet three to four times a day, best taken 15 to 30 minutes before meals or food, and if necessary at bedtime.

Sometimes your doctor may increase the dose to two tablets three to four times a day after you have taken Generic Motilium for 2 weeks.

You should not take more than a total of eight tablets in a single day.

Generic Motilium can be taken for up to 6 months.

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

Overdose

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

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Do not store in the bathroom, near the kitchen sink, or in other damp places. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Motilium 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 Motilium if you are allergic to Generic Motilium components.

Do not take Generic Motilium if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Motilium can harm your baby.

Do not take Generic Motilium if you have a tumour of the pituitary gland called prolactinoma; an increase in stomach or bowel contractions can harm you. For example, if you have had bleeding, a blockage or puncture in your gastrointestinal tract.

Do not take Generic Motilium if you are taking another medicine containing the active ingredient such as ketoconazole, fluconazole or voriconazole which is used to treat fungal infections.

Do not take Generic Motilium if you are taking an antibiotic containing the active ingredient erythromycin, clarithromycin or telithromycin.

Do not take Generic Motilium if you are taking another medicine containing the active ingredient amiodarone, which is used to treat fast heart rate.

Do not stop taking Generic Motilium suddenly.

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A retrospective cohort study was conducted, involving women who delivered live-born singletons (N = 21 914) at the WCH between January 2004 and December 2008. Women dispensed domperidone were identified using WCH pharmacy dispensing records. Maternal and infant clinical data were obtained from the WCH Perinatal Statistics Collection. Relationships between maternal/infant demographic and clinical variables and the use of domperidone were examined through univariate and multivariate logistic regression analyses.

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Ten patients with Parkinson's disease and urinary symptoms underwent urodynamic assessments before and after subcutaneous administration of the dopamine receptor agonist apomorphine. Voiding efficiency improved after apomorphine injection, with an increase in mean and maximum flow rates in nine patients and reduction in post-micturition residual volume in six. Although the effect on detrusor behaviour was variable, subcutaneous apomorphine may be of use in both the assessment and treatment of voiding dysfunction in patients with Parkinson's disease.

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A case is reported of neoplastic TSH hypersecretion in a 62-year-old man with severe hyperthyroidism and cardiovascular disease. He had been known to be hyperthyroid for 14 yr, and had been treated by thyreostatic drugs and subtotal thyroidectomy without satisfactory results. When he was referred to our Center, he was frankly hyperthyroid with both TSH (14 microU/ml) and thyroid hormone serum levels (TT4 24 micrograms/dl, TT3 370 ng/dl, FT41 7.9) above the normal range. alpha-subunit serum level was markedly increased (7.2 ng/ml), while beta-subunit was only 0.3 ng/ml. Skull X-ray showed an enlarged sella turcica with destruction of the dorsum and an intrasellar tumor was visualized on conventional and computer tomography. TSH response was absent after TRH and domperidone, while TSH serum levels decreased by 25% after bromocriptine. Methimazole therapy temporarily decreased serum thyroid hormones to normal levels, while TSH levels rose to 34 microU/ml, thus indicating that pituitary-thyroid feed-back was maintained at a higher set point. Surgical attempt failed because of cardiac problems during anesthesia. Radiotherapy plus methimazole was begun and TSH serum levels first increased markedly, up to 140 microU/ml, and then progressively decreased without reaching normal values. After methimazole withdrawal hyperthyroidism recurred.

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Symptom scores, stool data, and the transit of a standard, solid meal were measured in 25 patients with irritable bowel syndrome during baseline conditions and after four weeks treatment with placebo and domperidone in the form of a double-blind cross-over trial. All patients had previously undergone a comprehensive series of diagnostic investigations and had failed to respond to dietary supplementation with coarse wheat bran (10-30 g daily). Compared with placebo treatment, domperidone had no significant effect on gastric emptying, small bowel or whole gut transit times, stool weight, frequency, or consistency. Most symptoms improved significantly with both placebo and domperidone treatments, compared with the baseline period, but there was no significant difference between placebo and domperidone for any of the symptoms. Abdominal distension, however, was reported on more days per week during domperidone treatment (p = 0.02). The findings in this study do not support the use of domperidone in the management of irritable bowel syndrome.

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In Langendorff perfused rabbit hearts, domperidone significantly prolonged the action potential duration starting at 30 nM. It induced proarrhythmic TRIaD from 100 nM on. Since therapeutic free drug concentrations extend to 19 nM, the safety ratio for domperidone equals 100/19 = 5.25, i.e., far below the minimum safety ratio of 30. Hence, widespread use of domperidone cannot be without danger; especially since it is frequently used as an over the counter medication.

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Prospective randomised controlled trials (RCTs) of self- or parent-administered drug treatments in children (under 18 years of age) who had received a diagnosis of migraine were included.

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We applied the Caco-2VCR cells to a 96-well plate-based calcein AM extrusion assay. The Caco-2VCR cells were cultured as monolayers and incubated with calcein AM with/without addition of Pgp modulators. Fourteen known Pgp modulators were tested in the assay (chloropromazine, cyclosporin A, domperidone, digoxin, ivermectin, ketoconazole, loperamide, metoprolol, propranolol, progesterone, quinidine, quinine, verapamil and vincristine). For each compound an EC50 value was calculated. Protein and mRNA levels of the efflux transporters were analysed by Western blot and polymerase chain reaction techniques.

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In nonrestrained dogs that had not been given chemicals and that were in the fasted and fed state, gastroesophageal sphincter pressure (GESP) was measured; results were compared with GESP induced in the same dogs by drugs that modified activity at cholinergic, adrenergic, histaminic, and gastrin receptors. Atropine reduced GESP from 38.5 +/- 1.3 (mean +/- SE) and 55.5 +/- 2.0 mm of Hg to 11.3 +/- 2.0 and 14.5 +/- 2.4 mm of Hg in fasted and fed dogs, respectively. Histamine induced phasic contractions that were not affected by anticholinergics or cimetidine. Iphenhydramine eliminated the phasic contractions and reduced GESP to 18.2 +/- 3.9 mm of Hg. In fed dogs, diphenhydramine reduced GESP to 37.0 +/- 2.5 mm of Hg, but cimetidine did not. Pentagastrin induced increases in GESP that were inversely related to basal GESP. Pentagastrin given during histamine infusion eliminated histamine-induced phasic contractions. In fed dogs, metoclopramide increased GESP from 48.8 +/- 4.0 mm of Hg to 76.0 +/- 4.0 mm of Hg; this increment was eliminated by diphenhydramine. Administration of atropine after metoclopramide reduced GESP the same as for dogs given atropine alone. An adrenergic amine with only alpha-adrenergic effects induced phasic contractions, and an adrenergic amine with only beta-adrenergic effects reduced GESP. Blockers of alpha and beta effects did not change GESP in fed dogs. Domperidone induced phasic contractions that were eliminated by feeding. Serotonin increased GESP. Canine GESP may be maintained in fed dogs by chemicals interacting with cholinergic, histaminic, gastrin, and serotonin receptors, but not by chemicals interacting with adrenergic receptors.

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Intestinal motility is regulated by several neurotransmitters and neuropeptides including dopamine and acetylcholine as well as ghrelin. Metoclopramide and domperidone are long-standing treatment options for dysmotility, and erythromycin is suggested in selected patients. In the present study, we aimed to investigate the effects of mentioned prokinetics on ghrelin levels.

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The completion rate (CR) of small bowel capsule endoscopy (SBCE) has been reported at 81.3% to 84.8%. Prokinetic agents are used to increase CR and (theoretically) diagnostic yield (DY). Domperidone has not been widely used in SBCE; unlike metoclopramide, it lacks extrapyramidal adverse effects.

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Abstract The purpose of this study was to determine whether prolactin (PRL) could exert a negative feedback on it's own secretion during pregnancy and following ovariectomy, and to determine the possible mechanism by which this feedback acts. Implantation of ovine PRL into the arcuate nucleus-median eminence area of the hypothalamus completely inhibited the nocturnal PRL surge during pregnancy in the rat, and lowered baseline PRL to almost undetectable levels in the ovariectomized rat. When ovariectomized rats implanted with ovine PRL in the hypothalamus were injected with the dopamine receptor blocker domperidone the PRL response was significantly lower than in control rats implanted with albumin. Pregnancy increased the ability of domperidone to cause PRL release following ovine PRL implantation compared to what occurred in ovariectomized rats. These results suggest that PRL implantation increases the secretion of dopamine from the tuberoinfundibular neurons, resulting in a decrease in PRL secretion.

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A standardized protocol using subcutaneous apomorphine and rectal domperidone was used in two PD patients who underwent abdominal surgery. Excellent control of parkinsonian symptomatology was obtained without side effects. The simplicity of the protocol was emphasized in our second patient who required urgent reoperation; the surgery nursing staff was able to restart the apomorphine immediately without having to wait for neurological follow-up assessment.

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The curative group had better effects than the control group in lowering the blood sugar and the level of 5-HT(2A)R content (P < 0.01). And there was significant difference between the curative group and control group (P < 0.05).

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The effects of intravenous infusions of dopamine (0.1 to 1 mg kg-1h-1) and bromocriptine (10 to 40 micrograms kg-1h-1) on colonic motility were investigated in fasted dogs fitted with permanent strain gauges on the ascending, transverse and descending colon. Infused at rates of 0.5 and 1 mg kg-1h-1 during 1 h, dopamine immediately stimulated the motility of the descending colon; after a delay of 40 to 60 min this effect was balanced by an inhibition of the motility of the ascending and transverse colon. Bromocriptine infused intravenously at doses of 10 to 40 micrograms kg-1h-1 stimulated the motility of the whole colon but these effects were limited to the duration of the infusion (60 min). Both propranolol (0.5 mg kg-1) and tolazoline (2 mg kg-1) failed to block the effects of dopamine and bromocriptine whereas phentolamine (0.1 mg kg-1) and prazosin (0.2 mg kg-1) partially reduced the inhibitory effects of dopamine on the proximal colon. Haloperidol at doses higher than 0.2 mg kg-1 and domperidone blocked the bromocriptine-induced stimulation of colonic motility which was unaffected by previous treatment with alpha- and beta-adrenoceptor blocking agents. These results suggest that in the dog, dopamine and bromocriptine stimulate colonic motility through specific dopamine receptors. However, they suggest that the inhibitory effects of dopamine on the proximal colon which are blocked by dopamine antagonists are also partially due to an effect on alpha 1-adrenoceptors.

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Periodic breathing (PB) is an instability of the respiratory control system believed to be mediated principally by the peripheral chemoreceptors. We hypothesised that domperidone, a dopamine D(2)-receptor antagonist that increases carotid body sensitivity to O(2) and CO(2), would promote PB through an increase in the loop gain (LG) of the respiratory control system. Domperidone significantly increased controller gain for oxygen (p<0.05) and gave rise, following post-hyperventilation apnea, to an increased incidence of PB (14% vs. 86%), an increased PB epoch duration, and a decrease in duty ratio of PB (p<0.001); these changes are consistent with domperidone increasing LG. Although domperidone increased controller gain for CO(2) (p<0.05), the contribution of Pa(CO)(2) oscillations to the genesis of PB in the lamb remained small. We conclude that domperidone increases LG in the lamb via an increase in controller gain for oxygen. Our study demonstrates that a quantitative understanding of the factors that determine LG provides insight into the cause of PB.

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Ventilatory acclimatization to sustained hypoxia (VASH) is the time-dependent increase in ventilation that occurs during prolonged exposure to hypoxia. We tested the hypothesis that carotid body (CB) dopaminergic mechanisms are down-regulated during VASH, which would allow CB afferent discharge and ventilation to increase beyond the initial response to hypoxia. Domperidone (DOM; 1.0 mg.kg-1) was administered intravenously to block CB dopamine (DA) receptors after VASH was complete in awake goats. DOM caused a significant augmentation of the ventilatory response to hypoxia in acclimatized goats, failing to support the hypothesis. We conclude that inhibitory CB dopaminergic function is not significantly reduced following prolonged hypoxia, and that down-regulation of CB dopaminergic mechanisms may not be involved in VASH in the goat.

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A simple and sensitive liquid chromatography-tandem mass spectrometry method was developed and validated for determining domperidone in human plasma. The analyte and internal standard (IS; mosapride) were isolated from plasma samples by protein precipitation with methanol (containing 0.1% formic acid). The chromatographic separation was performed on an Xterra MS C(18) Column (2.1 x 150 mm, 5.0 microm) with a gradient programme mobile phase consisting of 0.1% formic acid and acetonitrile at a flow rate of 0.30 mL/min. The total run time was 4.0 min. The analyses were carried out by multiple reaction monitoring using the parent-to-daughter combinations m/z 426 --> 175 and m/z 422 --> 198 (IS). The areas of peaks from the analyte and IS were used for quantification of domperidone. The method was validated according to the FDA guidelines on bioanalytical method validation. Validation results indicated that the lower limit of quantification was 0.2 ng/mL, and the assay exhibited a linear range of 0.2-60.0 ng/mL and gave a correlation coefficient (r(2)) of 0.999 or better. Quality control samples (0.4, 0.8, 15 and 50 ng/mL) in six replicates from three different analytical runs demonstrated an intra-assay precision (RSD) 4.43-6.26%, an inter-assay precision 5.25-7.45% and an overall accuracy (relative error) of <6.92%. The method can be applied to pharmacokinetic and bioequivalence studies of domperidone.

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The goal of this study was to determine whether the dopamine D3 receptor in limbic structures plays a role in the shell-specific and dopamine-dependent display of turning behaviour in rats. When combined with the dopamine D1 receptor agonist (+/-)-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine-7,8-diol (SKF-38393, 5 micrograms), the putative dopamine D3 receptor agonist (+/-)-7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT, 1, 5 and 10 micrograms) elicited contralateral turning in a dose-dependent manner following unilateral injection into the shell, but not the core, of the nucleus accumbens. The turning pattern displayed was identical to that reported previously after intra-accumbens administration of the cocktail of SKF-38393 and the dopamine D2 receptor agonist quinpirole. The behaviour under study was dose-dependently attenuated by local administration of the dopamine D1 receptor antagonist R(+)-7-chloro-8-hydroxy-3- methyl-I-phroyl-2,3,4,5-tetrahydro-1H-3-benzazepine (SCH 23390: 10 and 100 ng), the dopamine D2 receptor antagonist domperidone (25 and 50 ng) or the dopamine D2/3 receptor antagonist l-sulpiride (5 and 25 ng). Combined blockade of both dopamine D1 and D2 receptors in the shell with a dose of either antagonist alone that produced just a moderate reduction (10 ng SCH 23390 and 50 ng domperidone) completely antagonized the turning behaviour elicited by the cocktail of SKF-38393 and 7-OH-DPAT. Replacing 7-OH-DPAT by another putative dopamine D3 receptor agonist,S(+)-(4aR, 10bR)-3,4,4a,10b-tetrahydro-4-propyl-2H,5H-[1]benzopyrano[4, 3-b]-1, 4-oxazin-9-ol (PD 128,907, 10 micrograms), in the cocktail did produce no turning behaviour at all. It is concluded that mesolimbic dopamine D3 receptors play no role in the dopamine-dependent and shell-specific turning behaviour: the contribution of 7-OH-DPAT in the cocktail of SKF-38393 and 7-OH-DPAT to the display of turning behaviour is solely due to its ability to activate dopamine D2 receptors.

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Swallowing disorders are common in Parkinson's disease but are of obscure and complex nature and pathophysiology. The effect of central dopaminergic stimulation on disordered swallowing is not well known. We studied the effects of apomorphine (in combination with domperidone) on buccolinguofacial motoricity and on various swallowing stages by using videofluoroscopy in eight patients with dysphagia. Swallowing abnormalities more frequently encountered were vallecular stasis (n = 7), fragmentation of the bolus (n = 7), and buccal stagnation of the bolus. Apomorphine improved vallecular stasis and fragmentation in about half the cases and improved buccal stagnation in all cases. Direct laryngeal penetration was found in three cases and improved in two of them. The total swallowing duration was improved by apomorphine in a subset of patients (n = 5). This improvement correlated with an improvement of the buccolinguofacial motoricity and was combined with an improvement of pharyngeal transit time. Thus central dopaminergic stimulation by apomorphine improved swallowing in a subgroup of patients, mainly in its early stages.

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Gastroparesis is a disorder of gastric emptying that occurs in the absence of mechanical obstruction. Its cardinal features include nausea, vomiting, bloating, early satiety and discomfort. Weight loss, dehydration, electrolyte disturbances and malnutrition may develop in severe cases. The majority of cases is idiopathic, long standing diabetes mellitus is responsible for about 25-30% of cases. Diabetic gastroparesis may render glucose control extremely difficult, its treatment represents a major challenge. Besides frequent, small meals and psychological support, several drug options are available, however, their efficacy is limited and only a few randomized studies have been performed to date. Prokinetic agents (erythromycin, domperidone, metoclopramide) and antiemetics (phenothiazines, serotonin antagonists, butyrophenones) are the most wide-spread medicaments. Among the novel, recently developed agents, 5-HT4 serotonin receptor agonists and dopamine D2 receptor antagonists are the most promising. Injection of botulinum toxin into the pyloric sphincter resulted in faster gastric emptying and symptom alleviation in some studies. Gastric electric stimulation appears to be one of the most effective options, both low and high-frequency stimulation may alleviate symptoms. Gastrostomy/jejunostomy and other surgical interventions are considered as "last resort".

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The use of antiemetics for vomiting in acute gastroenteritis in children is still a matter of debate. We conducted a double-blind randomized trial to evaluate whether a single oral dose of ondansetron vs domperidone or placebo improves outcomes in children with gastroenteritis. After failure of initial oral rehydration administration, children aged 1-6 years admitted for gastroenteritis to the pediatric emergency departments of 15 hospitals in Italy were randomized to receive one oral dose of ondansetron (0.15 mg/kg) or domperidone (0.5 mg/kg) or placebo. The primary outcome was the percentage of children receiving nasogastric or intravenous rehydration. A p value of 0.014 was used to indicate statistical significance (and 98.6% CI were calculated) as a result of having carried out two interim analyses. 1,313 children were eligible for the first attempt with oral rehydration solution, which was successful for 832 (63.4%); 356 underwent randomization (the parents of 125 children did not give consent): 118 to placebo, 119 to domperidone, and 119 to ondansetron. Fourteen (11.8%) needed intravenous rehydration in the ondansetron group vs 30 (25.2%) and 34 (28.8%) in the domperidone and placebo groups, respectively. Ondansetron reduced the risk of intravenous rehydration by over 50%, both vs placebo (RR 0.41, 98.6% CI 0.20-0.83) and domperidone (RR 0.47, 98.6% CI 0.23-0.97). No differences for adverse events were seen among groups. In a context of emergency care, 6 out of 10 children aged 1-6 years with vomiting due to gastroenteritis and without severe dehydration can be managed effectively with administration of oral rehydration solution alone. In children who fail oral rehydration, a single oral dose of ondansetron reduces the need for intravenous rehydration and the percentage of children who continue to vomit, thereby facilitating the success of oral rehydration. Domperidone was not effective for the symptomatic treatment of vomiting during acute gastroenteritis.

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Hyperprolactinaemia, as induced by pituitary homografts under the kidney capsule, was accompanied by an inhibition of development of gastric ulcers following the application of cold-plus-restraint stress in male rats. This effect was mimicked by intracisternal administration of a low dose of the hormone. Peripheral injection of the dopamine receptor antagonist, domperidone, also inhibited the development of stress-induced ulcers. However, no effect was found after peripheral injection of another dopamine receptor antagonist, haloperidol. This latter drug appeared to antagonize the cytoprotective effect of prolactin (PRL) on stress-induced ulcers. Furthermore, peripheral injection of the prostaglandin synthesis inhibitor, indomethacin, increased the incidence of gastric ulcers in hyperprolactinaemic rats subjected to cold -plus-restraint stress. These data suggest that the cytoprotective effect of PRL on development of gastric ulcers in stressed animals may involve both central (i.e. dopamine transmission) and peripheral (i.e. prostaglandin synthesis) mechanisms.

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At T0 no statistical difference was found for each symptom between medical device and domperidone. At T1 both treatments significantly improved in respect to baseline values all the evaluated gastrointestinal symptoms (P<0.5 for all comparisons) except for vomiting. No difference in gastrointestinal symptoms between the two treatments was found at T1. Regarding SF-36 evaluation, at T0 no statistical differences were found for each SF-36 parameter between the two regimens. At T1 both treatments significantly improved most of the evaluated SF-36 parameters in respect to baseline values. No difference in SF-36 parameters between the two treatments was found at T1.

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The present investigation was undertaken with the objective of formulating mouth dissolving film(s) of the antiemetic drug Domperidone to enhance the convenience and compliance by the elderly and pediatric patients. Domperidone is a drug of choice in case of nausea and vomiting produced by chemotherapy, migraine headaches, food poisoning and viral infections. It causes dopamine (D2 and D3) receptor blockage both at the chemoreceptor trigger zone and at the gastric level. It shows high first pass metabolism which results in poor bioavailability (10-15%). In view of high first pass metabolism and short plasma half-life it is an ideal candidate for rapid release drug delivery system. The solid dispersions of Domperidone were prepared with the use β-cyclodextrin in various ratios (1:1, 1:2, 1:3) and solubility study was performed to determine the ratio in which solubility of Domperidone was highest (1:3). The selected solid dispersions were then utilized for the preparation of film by solvent casting method utilizing HPMC E15 as a film forming agent and PEG-400 as plasticizer. Five formulae were prepared and were evaluated for their in vitro dissolution characteristics, in vitro disintegration time, and their physico-mechanical properties. The promising film (F1) showed the greatest drug dissolution (more than 75% within 15 min), satisfactory in vitro disintegration time (45 sec) and physico-mechanical properties that are suitable for mouth dissolving films.

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The study was completed by 22 women in the domperidone group and 23 in the placebo group. Compared with day 0, mean increases in milk volume per participant collected on days 1, 2, 3, and 4 were significantly higher in the domperidone (13.6 ± 23.2 mL, 68.5 ± 71.9 mL, 144.5 ± 122.3 mL, and 191.3 ± 136.1 mL) than in the placebo (2.5 ± 4.6 mL, 24.5 ± 26.5 mL, 72.1 ± 55.6 mL, and 91.4 ± 60.3 mL) group. Minor adverse effects were reported by 7 women in the domperidone group.

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Induced spawning of C. batrachus was conducted at different Ovaprim dose and latency period combinations to observe the deformed larvae among the hatchlings. For the purpose, four doses of Ovaprim (0.5, 1.0, 1.5 and 2.0 ml/kg body weight) and five latency periods (11, 14, 17, 20 and 23 hr) were considered in 20 different combinations. There were no deformed larvae in the females injected with all four doses and stripped at 11 hr latency, as the eggs did not hatch. The percentage of deformed larvae (4-7%) did not vary significantly at 1.0-2.0 ml dose level in combination with 14-17 hr latency periods. While increasing the latency period beyond 17 hr at 1-1.5 ml dose level, the percentage of deformed larvae increased significantly and touched as high as 11%. The results indicated that 1-1.5 ml dose in combination with 14-17 hr latency are suitable to reduce the deformed larvae among the hatchlings during induced spawning of C. batrachus.

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Systemic administration of apomorphine, angiotensin II, neurotensin and leucine-enkephalin induces emesis in dogs in a dose-dependent fashion. Receptors for Leu-enkephalin and angiotensin II but not apomorphine show receptor desensitization, such that a second systemic administration 5 min after the first is ineffective. Domperidone blocked the emetic response to apomorphine but not to Leu-enkephalin or angiotensin II. Naloxone selectively blocked the Leu-enkephalin response, while saralasin blocked responses to both angiotensin II and Leu-enkephalin, but not apomorphine. Chlorpromazine prevented the emetic response to all agents, suggesting a dopamine receptor in the emetic pathway on the brain side of the blood-brain barrier. In dogs with ablation of the area postrema the emetic response to apomorphine and all peptides was prevented.

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Intravenous (i.v.) infusions of SCH 23390 (R-(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7- ol) produced dose-related antagonism of dopamine (DA)-induced renal vasodilation in phenoxybenzamine-treated dogs at infusion rates of 0.05, 0.15, and 0.5 microgram/kg/min. The highest rate of infusion, 0.5 microgram/kg/min, resulted in pronounced antagonism of this DA1-receptor-mediated response. In contrast, a 10 times higher infusion rate, 5 micrograms/kg/min, did not antagonize the following DA2-mediated responses: increase in femoral blood flow produced by apomorphine and piribedil in untreated dogs; and N,N-di-n-propyl DA (DPDA)-induced inhibition of the tachycardia produced by cardiac accelerator nerve stimulation. Infusions of 0.5 micrograms/kg/min or greater of SCH 23390 did not affect the actions of agonists of alpha1-, alpha2-, beta1-, and beta2-adrenergic, histamine, serotonin, and cholinergic receptors, or the vasodilation produced by bradykinin. At the infusion rates used in these studies, SCH 23390 did not affect arterial blood pressure or heart rate. These data indicate that SCH 23390 is the most specific and selective antagonist of DA1 receptors thus far described. Accordingly, SCH 23390 should be extremely useful in investigations of potential physiological and pathological roles of DA and in the classification of DA receptors.

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Modulation of the hypoxic ventilatory response (HVR) by dopamine D(2)-receptors (D(2)-R) in the carotid body (CB) and central nervous system (CNS) are hypothesized to contribute to ventilatory acclimatization to hypoxia. We tested this with blockade of D(2)-R in the CB or CNS in conscious rats after 0, 2 and 8 days of hypoxia. On day 0, CB D(2)-R blockade significantly increased VI and frequency (fR) in hyperoxia (FI(O(2))=0.30), but not hypoxia (FI(O(2))=0.10). CNS D(2)-R blockade significantly decreased fR in hypoxia only. On day 2, neither CB nor CNS D(2)-R blockade affected VI or fR. On day 8, CB D(2)-R blockade significantly increased hypoxic VI and fR. CNS D(2)-R blockade significantly decreased hypoxic VI and fR. CB and CNS D(2)-R modulation of the HVR decreased after 2 days of hypoxia, but reappeared after 8 days. Changes in the opposing effects of CB and CNS D(2)-R on the HVR during chronic hypoxia cannot completely explain ventilatory acclimatization in rats.

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The objective of the present experiments was to determine the specific receptor subtype through which dopamine (DA) receptor agonists relax the lower esophageal sphincter in vitro. Opossum lower esophageal sphincter smooth muscle strips were placed in oxygenated Krebs' solution containing propranolol and cocaine. The tissues were placed at a tension that gave maximum relaxation to electrical field stimulation and were then pretreated with phenoxybenzamine. The effects of DA, and the DA receptor agonists epinine and apomorphine were determined. In addition, agonist responses were studied in the presence of the selective DA2 receptor antagonist domperidone, a mixed DA1/DA2 receptor antagonist metoclopramide, and the selective DA1 receptor antagonists bulbocapnine and SK&F 83566. The DA agonists relaxed the smooth muscle strips in the following order of potency: DA greater than epinine greater than apomorphine. Domperidone did not antagonize DA- or apomorphine-induced relaxation. Metoclopramide failed to alter DA-induced relaxation. Bulbocapnine and SK&F 83566 significantly inhibited the relaxation induced by DA. These data indicate that DA-induced lower esophageal sphincter relaxation in vitro is mediated by DA1 receptors.

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The in vitro dopamine-D2 receptor binding profiles of two substituted benzamides (3H-sulpride and 3H-raclopride) and two butyrophenones (3H-spiperone and 3H-domperidone) were compared. 3H-Raclopride, 3H-domperidone and 3H-sulpride labelled approximately the same number of binding sites in the rat striatum, while 3H-spiperone labelled a higher number of binding sites. This latter finding was suggested to be due to the labelling of 5-HT2 receptors in addition to the dopamine-D2 binding sites since the labelling of these 5-HT2 receptors with 3H-spiperone could be avoided by the addition of the 5-HT2 receptor antagonist ketanserin. The inhibition constants (Ki) of the unlabelled compounds were similar to the Kd values obtained in the saturation analyses with 3H-raclopride, 3H-domperidone and 3H-sulpiride but were significantly higher when 3H-spiperone was used as radioligand. Addition of ketanserin to 3H-spiperone made the Ki values more similar to those obtained with the other radioligands. The implications of these findings in testing antidopaminergic activity is discussed.

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Evidence is presented that a low dose of peripherally administered N,N-dipropylamino-5,6-dihydroxytetralin (DiPr-5,6-ADTN) specifically labels dopamine (DA) receptors in rat brain. Concentrations of this potent DA receptor agonist were determined by a highly selective method using reversed phase liquid chromatography and amperometric detection. The binding characteristics satisfy all criteria regarding saturability, stereospecificity, regional distribution and relation with pharmacological effects that are associated with DA receptor interactions. A rough estimation of the density of binding sites in the striatum resulted in values of 60-70 pmol/g. Lesioning the nigrostriatal pathway does not significantly alter the amount of ligand bound, nor do pretreatments with serotonergic, alpha-adrenergic or beta-adrenergic antagonists. DiPr-5,6-ADTN has thus been shown to be a useful ligand for labeling central DA receptors and a powerful tool in the study of DA-ergic mechanisms.

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The goal of this study was to determine whether the dopamine D3 receptor in limbic structures plays a role in the shell-specific and dopamine-dependent display of jaw movements in rats. When combined with the dopamine D1 receptor agonist (+/-)-6-chloro-7,8-dihydroxy-3-allyl-1- phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine (SKF 82958, 5 micrograms), the putative dopamine D3 receptor agonist (+/-)-7-hydroxy-N, N-di-n-propyl-2-aminotetralin (7-OH-DPAT, 10 micrograms) produced repetitive jaw movements following injection into the shell, but not the core, of the nucleus accumbens. This behaviour was only partially inhibited by local blockade of dopamine D1 receptors (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine, SCH 23390, 500 ng), dopamine D2 receptors (domperidone, 50 and 100 ng) or dopamine D2/3 receptors (l-sulpiride, 25 ng). Combined blockade of both dopamine D1 and D2 receptors in the shell completely antagonized the jaw movements elicited by the cocktail of SKF 82958 and 7-OH-DPAT. Replacing 7-OH-DPAT by another putative dopamine D3 receptor agonist, S(+)-(4aR, 10bR)-3,4,4a,10b-tetrahydro-4-propyl-2H,5H-[I]benzopyrano[4, 3-b]-1, 4-oxazin-9-ol (PD 128,907, 10 micrograms), in the cocktail did not produce jaw movements, when administered into the shell. Injection of the cocktail of SKF 82958 and 7-OH-DPAT into the ventrolateral striatum, which contains nearly no dopamine D3 receptors, also elicited jaw movements. It is concluded that mesolimbic dopamine D3 receptors play no role in the dopamine-dependent and shell-specific jaw movements: the contribution of 7-OH-DPAT in the cocktail of SKF 82958 and 7-OH-DPAT to the display of jaw movements is solely due to its ability to activate dopamine D2 receptors.

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Inflammatory edema was induced by carrageenan in male rats, and hyperprolactinemia was induced by injections of the dopamine receptor antagonist domperidone. The volume of inflammatory edema was measured by plethysmography after carrageenan injection. Additionally, the effects of hyperprolactinemia on body weight and serum corticosterone levels were evaluated.

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buy motilium boots 2017-01-28

Domperidone is often used to promote lactation among women motilium buy who have difficulty breastfeeding.

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Studies were carried motilium buy out on 22 healthy male volunteers to investigate whether intravenous administration of either the opiate antagonist, naloxone, or the dopamine antagonist, domperidone, or the alpha 2-adrenoreceptor antagonist, idazoxan, could reverse the delay in gastric emptying induced by ileal infusion of lipid emulsion. Ileal infusion of 50% lipid emulsion significantly delayed the rate of gastric emptying compared with ileal infusion of isotonic saline (P less than 0.01). Intravenous infusion of naloxone (20 micrograms kg-1 hour-1) or prior administration of either intravenous domperidone (20 mg) or idazoxan (0.2 mg kg-1) did not inhibit the delay in gastric emptying induced by ileal infusion of lipid emulsion. These observations indicate that feedback regulation of gastric emptying by ileal lipid does not appear to be mediated by either dopaminergic or enkephalinergic neurons, nor by alpha 2-adrenoreceptors.

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A differential pulse voltammetric method was described for the determination of domperidone. The method was based on the anodic oxidation of domperidone on a glassy carbon electrode at +0.64 V vs. SCE in Britton-Robinson buffer solution of pH 2.3. The reversibility of the oxidation was tested by cyclic voltammetry; the electrode process is irreversible and Parlodel Cost diffusion-adsorption controlled. Calibrations are linear over the range 1.0 x 10(-6)-2.0 x 10(-5) M of domperidone with a detection limit of 4.0 x 10(-7) M. The method was applied, without any interference from the excipients, to the determination of the drug in a tablet dosage form.

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To investigate the influence Deltasone Dose Pack of omeprazole on the pharmacokinetics of domperidone given as free base and maleate salt.

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The author discusses the Cymbalta Itching Remedy role of prokinetic agents, such as bethanechol, metoclopramide, domperidone, and cisipride in the management of gastroesophageal reflux disease. These agents address the upper gastrointestinal motility disturbances that contribute to this disease and therefore have an important role in the acute and long-term medical management of reflux esophagitis.

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1. Pharmacological blockade of DA-2 receptors causes a significantly higher epinephrine (E) response to physical exercise in normal man. 2. The present study was undertaken to evaluate whether dopaminergic modulation of E secretion is present also for a stimulus such as glucagon which acts directly on chromaffin cells. 3. Seven normal males were studied in a single blind randomized manner on two separate occasions, after pre-treatment with placebo or domperidone (DMP; 20 mg orally). Plasma E and norepinephrine, plasma prolactin, heart rate and blood pressure were measured on two separate occasions (placebo vs DMP) before and after a glucagon (1 mg i.v.) stimulation test. 4. Glucagon caused an increase in plasma E either after placebo (P = 0.043) or after domperidone (P = 0.012). DMP administration caused a significant increase in plasma E (P = 0.0008). Absolute increase in plasma E after glucagon was significantly higher after DMP than after placebo (P = 0.030). 5. As the dopaminergic modulation of human adrenal medulla is confirmed also for a stimulus acting directly on chromaffin cells, the results of the present study suggest that the DA-2 receptors responsible for the modulation are located on Azulfidine Sulfasalazine Dosage medullary cells.

motilium uk buy 2015-03-26

In this review we have looked at the evidence for Cialis Buy Online the pharmacological treatment of lactation deficiency. Five RCTs (n = 166) of metoclopramide found no effect on lactation and two RCTs (n = 26) of older date and lesser quality found significant effect. One RCT (n = 51) of syntocinon found no effect on lactation and two older RCTs (n = 60) of lesser quality found significant effect. Three RCTs (n = 105) found significant effect of domperidone on lactation. Education on breastfeeding is important to avoid the need for pharmacological treatment.

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Four rapid, simple, reproducible and sensitive methods (A-D) for assaying domperidone (I) and metoclopramide (II) in a bulk sample and in dosage forms were investigated. The first and second methods, A and B, are based on the oxidation of I and/or II by Fe3+ in the presence of o-phenanthroline (o-phen) or bipyridyl (bipy). The formation of tris-complex upon reactions with Fe3+-o-phen and/or Fe3+-bipy mixture in Sinemet Cr Generic an acetate buffer solution of the optimum pH-values was demonstrated. Methods C and D involve the addition of excess Ce4+ and the determination of unreacted oxidant by a decrease of the red color of chromotrope 2R (C2R) at a suitable lambda(max) of 528 nm for method C, or a decrease in the orange pink color of Rhodamine 6G (Rh6G) at a suitable lambda(max) value of 525 nm for method D. A regression analysis of Beer-Lambert plots showed a good correlation in the concentration range of 0.2-5.8 microg ml(-1). The apparent molar absorptivity, Sandell sensitivity, detection and quantification limits were calculated. For a more accurate analysis, the Ringbom optimum concentration ranges are 0.35-5.6 microg ml(-1). The developed methods were successfully applied to the determination of domperidone and metoclopramide in bulk and pharmaceutical preparations without any interference from common excipients.

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Apomorphine (0.05 mg/kg intravenously) was given to conscious dogs, and gastrin levels were measured in peripheral venous blood with a radioimmunoassay. Apomorphine induced an increase of gastrin levels which peaked at 5 min. The peripheral dopamine D-2/DA2 receptor antagonist domperidone (0.2 mg/kg), but not halopemide (0.1-1 mg/kg) nor the D-1/DA1 receptor antagonist SCH 23,390 (0.1 mg/kg), blocked the gastrin response to apomorphine. Both domperidone Indocin Oral Suspension and halopemide, but not SCH 23,390, blocked the apomorphine-induced vomiting. These results suggest that apomorphine increases gastrin levels by an action at D-2/DA2 receptors, which are situated outside the blood brain barrier and differ from the receptor inducing the vomiting.

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Behavioral hyposensitivity to repeated apomorphine administration has been observed in fluctuating parkinsonian patients. To investigate whether a similar phenomenon occurs in patients never treated with levodopa, we studied the response to apomorphine in 20 de novo patients with Parkinson's disease. Six patients showed no or minimal improvement after apomorphine injections (maximal dose 3.5 mg). Fourteen patients responded and were then given up to four repeated subcutaneous injections of apomorphine [minimal effective dose (MED)]. The responses of de novo patients were compared with responses in 10 patients with motor fluctuations previously studied by the same protocol. There was no significant difference in latency and duration of motor responses after repeated apomorphine injections in de novo patients. MED was similar in de novo and fluctuating patients, but duration of improvement induced by each apomorphine bolus was longer in the de novo group. These results indicate that response duration to apomorphine is longer in previously untreated patients and that behavioral tolerance associated with pulsatile dopaminergic stimulation by apomorphine occurs mainly in Inderal Skyrim Review patients with more advanced disease under chronic levodopa therapy.

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Domperidone and metoclopramide effectively reduce the symptoms Nolvadex Generic of diabetic gastroparesis; CNS side effects are more pronounced with metoclopramide.

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In a double-blind cross-over study over eight weeks two groups of 24 patients each with symptoms of chronic postprandial dyspepsia received during the first four-week period either 10 mg domperidon t.i.d. or placebo. After four weeks the medication was exchanged. Despite some improvement of symptoms under placebo, statistical analysis revealed a significantly higher improvement rate after domperidon.

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The incidence of dyspepsias and emesis occurring either as accompanying symptoms of gynaecological operations or as independent clinical conditions, therapeutic means for controlling these conditions and the mechanism of action and clinical usefulness of the dopamine antagonist domperidone have been discussed. The observations with this drug in 68 women suffering from dyspepsia and in 94 cases of emesis of different etiology have been analysed. The author stated that Motilium is the drug of choice in the treatment of complaints due to motility disorder of the upper gastroduodenal tract, that the patients tolerate the drug well, and that it's use does not hinder the treatment of the primary gynaecological disease, pre-operative therapy, anaesthesia, and postoperative care of the patients. Its antiemetic effect depends on the time of intake which is a disadvantage of oral application.

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Complications associated with the use of antiparkinsonian drugs make PD management more difficult given the need for antidopaminergic therapy, which worsens motor functioning in patients with PD. For psychosis, clozapine is the only atypical antipsychotic that has proven effective without worsening motor function in PD patients. However, its use requires the monitoring of agranulocytosis. Newer atypical antipsychotics such as quetiapine have been claimed to be safe in terms of motor functioning, but evidence about their effectiveness is not compelling. The emergency treatment of psychosis in PD would require parenteral administration, only available for olanzapine and ziprasidone. However, no randomized controlled trials have been conducted to establish the efficacy and safety in this setting. For nausea and vomiting, very little domperidone crosses the blood-brain barrier. As a result, the risk of developing extrapyramidal adverse effects is minimal. Metoclopramide blocks central dopamine receptors and worsens motor parkinsonian symptoms. Chlorpromazine, the first-line treatment of intractable hiccups, is contraindicated in PD. Baclofen could be considered as a first-line alternative.

buy motilium usa 2016-08-17

Experiments were designed to investigate the biochemical properties of binding sites for [3H]spiroperidol ([3H]SPD) solubilized from canine caudate and to define the effect of detergent on the binding of the radioligand. Extraction of canine caudate with 0.75-1.0% digitonin was found to generate the maximum yield of binding sites for [3H]SPD while minimizing extraction of membrane proteins. Although binding sites were solubilized with 1.0% digitonin, a 10-fold reduction in detergent concentration was necessary to achieve maximal binding of [3H]SPD. The rank order of affinity for agonists and antagonists was consistent with the pharmacologic properties of the D2 subtype of the dopamine receptor. However, the binding of antagonists was found to be complex. Studies with some preparations of pooled canine caudate resulted in competition curves for the D2-selective antagonists domperidone and sulpiride that best fit a single-site model. Other preparations exhibited biphasic inhibition curves with these antagonists. The class of binding sites for [3H]SPD with low affinity for D2-selective antagonists constituted as much as 30-40% of the binding sites. Enrichment of solubilized binding sites for [3H]SPD was achieved by size exclusion HPLC followed by adsorption to DEAE-Sephadex and elution with buffer of increasing ionic strength. Enrichment of binding sites was accompanied by a decrease in the affinity of solubilized sites for [3H]SPD.

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Responses to dopamine were compared in helical strips of human gastroepiploic arteries (proximal portion) and their epiploic branches (distal portion), partially contracted with prostaglandin F2 alpha. Dopamine produced a dose-related contraction in the proximal arteries, which was reversed to a relaxation by treatment with phentolamine. On the other hand, the distal arteries responded to low concentrations of dopamine with relaxations and to high concentrations with contractions. The relaxant response was selectively suppressed by treatment with droperidol and reversed to a contraction by SCH23390, but was not influenced by domperidone and propranolol. The amine-induced relaxation was not reduced by removal of the endothelium. The distal arteries, in which dopamine elicited a relaxation, responded to norepinephrine with dose-related contractions, which were suppressed by phentolamine but were not reversed to relaxations. It may be concluded that dopamine contracts human gastroepiploic arteries of the proximal portion, due to a predominant activation of alpha-adrenoceptors, and dilates the distal arteries by acting preferentially on dopaminergic DA1-receptors, possibly residing in smooth muscle. In the distal arteries, the ability of norepinephrine to activate alpha-adrenoceptors appears to be evidently higher than that of dopamine.

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In humans, behavioral dopamine supersensitivity occurs in schizophrenia and in Parkinson's disease. In animals, behavioral dopamine supersensitivity is consistently associated with increased dopamine D2(High) receptors in homogenized striata in vitro. Because D2(High) receptors have not yet been detected in intact cells, we used [(3)H]domperidone to detect D2(High) sites in intact rat anterior pituitary adenoma culture cells. Although [(3)H]raclopride and [(3)H]spiperone did not detect D2(High) receptors in intact cells or in rat fresh striatal slices, [(3)H]domperidone readily detected D2(High) receptors, warranting an in vivo search for D2(High) variations in human diseases.

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Nausea is common in patients with migraine. A number of antiemetic drugs can be useful in migraine treatment, and those with a prokinetic action (metoclopramide and domperidone) may also improve gastrointestinal absorption of analgesics and triptans during a migraine attack. In addition to providing headache relief, the triptans are very effective in relieving migraine-associated nausea. For migraine patients with nausea and/or vomiting severe enough to interfere with the use of oral medications, alternative drug delivery methods can be used. These include the injectable, intranasal and rectal suppository routes, and specialized oral medications such as sublingual tablets and oral wafers that dissolve in the mouth. Fortunately, effective medications that use some of these alternative delivery routes have become more available over the past several years.

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Genetic characteristics associated with response to domperidone therapy included polymorphisms in the drug transporter gene ABCB1, the potassium channel KCNH2 gene, and α1D--adrenoceptor ADRA1D gene. Age was associated with a beneficial response to domperidone. If verified in a larger population, this information might be used to help determine which patients with gastroparesis might respond to domperidone and avoid treatment in those who might develop side-effects.

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These findings clearly indicate that the two products are bioequivalent in terms of rate and extent of drug absorption. Both preparations were well tolerated with no adverse reactions throughout the study.

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A low dose of dopamine (1 microgram/min/kg) infused for 3 h, which is without systemic hemodynamic effects in normal subjects, increased the renal blood flow and renal production of prostacyclin (PGI2). This action was blocked by metoclopramide as well as by either of two cyclooxygenase (CO) blockers, but effects were not altered by administration of the alpha 1 blocker prazosin. Much of the effect of dopamine (DA) is apparently via the DA1 receptor, since fenoldopam (0.1 microgram/min/kg) reproduced these actions. However, although fenoldopam increased glomerular filtration rate and urinary Na+, CO blockers were without effect. In contrast neither DA or fenoldopam infusions changed either renal blood flow or PGI2 in a group of patients with essential hypertension. Renin secretion was shown to be increased via DA1 receptor activation both in humans and rat renal tissue. The DA2 receptor may also play a role since domperidone can reduce renal blood flow.

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Levo-sulpiride is a substituted benzamide with antiemetic activity 3-8 times more potent than the racemic form and the d-isomer. Its mode of action is partially central (inhibition of dopaminergic receptors at the trigger zone for vomiting) and partially peripheral (normalization of motor activity of stomach and gall-bladder). The drug was found effective in the prevention of chemotherapy-induced and post-operative vomiting as well as in the treatment of nausea and vomiting during hepatic, biliary and gastroduodenal disorders, organic and functional dyspepsia, motion sickness and vertigo. Levo-sulpiride is at least as effective as domperidone, antihistamines and neuroleptic agents. Compared with the latter drugs and with d-sulpiride and the racemus, l-sulpiride is much better tolerated. Drowsiness is reported only at high doses, and no clinical signs of hyperprolactinaemia are observed, even after prolonged treatment.

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In the subgroups of patients with GERD + DM 1 and GERD + DM 2, received treatment with IG complaints on heartburn, regurgitation, odynophagia relieved significantly earlier then in the subgroups treated with DP. After 4 weeks of therapy, decreasing in the number of gastroesophageal refluxes, number of patients with erosive esophagitis B level, and normalization of the motility of the stomach were significantly higher in the groups of GERD + DM 1 and GERD + DM 2 received treatment with IG when compared with the subgroup of PD. There were no side effects of prokinetics.

buy motilium australia 2016-03-18

A dopamine agonist, bromocriptine, and several dopamine antagonists, domperidone, haloperidol, floropipamide and chlofluperol, were studied for their effects on the ocular blood flow. Both domperidone and haloperidol are ocular hypotensive agents and are able to increase the ocular blood flow significantly. Floropipamide had little effect on the intraocular pressure (IOP), yet it reduced the ocular blood flow markedly. Chlofluperol is an ocular hypertensive agent, yet it increased the ocular blood flow significantly. Although bromocriptine lowered the IOP, it did not affect the ocular blood flow. These results indicate that the changes of ocular blood flow are independent of the changes of the IOP. Therefore, it is critical to develop antiglaucoma agents which can increase retinal and choroidal blood flow in addition to lowering the IOP.

buy motilium usa 2016-12-03

To retrospectively analyze the individual risk factors for radioactive iodine (RAI)-associated nausea and vomiting, and to examine the anti-emetic effect of ramosetron (5-hydroxytryptamine-3 receptor antagonist) in RAI therapy. Patients with differentiated thyroid carcinoma who underwent first-time RAI therapy at Nagasaki University Hospital between January 2009 and 2013 were included (N = 81). As a routine treatment, all patients were administered 30 mg of domperidone per day. Patients who underwent RAI therapy between April 2011 and January 2013 were also administered 0.1 mg of ramosetron per day in addition to domperidone. Nausea and vomiting were evaluated based on Common Terminology Criteria for Adverse Events version 4.0. RAI-associated nausea and vomiting of any grade were seen in 37.0 and 6.2 % of patients in total, respectively. Moderate to severe nausea (grade 2–3) was seen in 22.2 % of patients and associated with the dose of RAI per body weight (odds ratio = 1.046, p = 0.013), but not with the use of ramosetron, in multivariate logistic regression analysis. We have identified the dose of RAI per body weight to be an individual risk factor associated with moderate to severe RAI-associated nausea. This study failed to show that the combined use of ramosetron and domperidone reduced the frequency of RAI-associated nausea and vomiting.

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We confirmed a risk of cardiac adverse event related to prolongation of the QT interval with domperidone and setrons. These results suggest caution when prescribing antiemetics and encourage systematic reporting of adverse cardiac effects observed with these molecules.

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Tertiary level neonatal intensive care unit (NICU).

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Prolactin secretion and biological activity have been investigated in 20 females with persistent idiopathic galactorrhoea who had normal resting serum prolactin levels at presentation. Results were compared with those in 34 normal controls. Hyperprolactinaemia, which was persistent in one and intermittent in the other, developed in two patients over an observation period of 1.5 to 8.5 years. Resting prolactin levels stayed normal in the remaining eighteen who were further investigated. Menstruation was disordered in only six of the 18, while ovulation occurred (serum progesterone greater than 20 nmol/l) in all seven patients who were studied over a 5 week period. Serum prolactin concentrations over 24 h were similar in patients and controls (24 h mean +/- SEM prolactin, 288 +/- 36 mU/l, patients, n = 7; 291 +/- 21 mU/l, controls, n = 9) as were prolactin levels estimated twice weekly for 5 weeks. Prolactin responses to thyrotrophin-releasing hormone, 200 micrograms (at 20 min, 2417 +/- 658 mU/l, patients, n = 7; 2113 +/- 424 mU/l, controls, n = 8), the dopamine antagonist, domperidone, 10 mg (at 30 min, 5949 +/- 536 mU/l, patients, n = 7; 5858 +/- 460 mU/l, controls, n = 8) and insulin-induced hypoglycaemia (at 60 min, 1441 +/- 551 mU/l, patients, n = 7; 1298 +/- 183 mU/l, controls, n = 7) were similar in patients and controls. Two different radioimmunoassays using two different antisera gave similar estimates of serum prolactin levels and prolactin bioactivity in serum was normal in an in-vitro bioassay based on the ability of prolactin to stimulate proliferation of Nb2 node rat lymphoma cells (basal bioassayable prolactin, patients 355 +/- 43 mU/l, n = 10; controls 348 +/- 64 mU/l, n = 7). Metabolic abnormalities similar to those previously noted in hyperprolactinaemia were observed in the patients' 24 h profiles. These included mild hyperglycaemia (24 h mean +/- SEM glucose, 5.47 +/- 0.08 mmol/l, patients; 5.05 +/- 0.14 mmol/l, controls; P less than 0.05) and elevations in circulating lactate, pyruvate and alanine. Blood glycerol was decreased (24 h mean +/- SEM, 0.044 +/- 0.004 versus 0.058 +/- 0.004 mmol/l, P less than 0.05). In the majority of patients with idiopathic galactorrhoea, prolactin concentrations, regulation of secretion and bioactivity in vitro are normal. The galactorrhoea and metabolic abnormalities suggest increased tissue sensitivity to the lactogenic and metabolic actions of prolactin, while ovarian cyclical function is relatively spared.

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To define the effective dose of cabergoline and to evaluate the tolerability and efficacy of cabergoline in patients with restless legs syndrome (RLS).

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Previously, we demonstrated that dopamine (DA) stimulates GH release from the pituitary of goldfish, and this action is mediated by D1-like receptors. In the current study, we have provided evidence for the presence of D1-specific binding sites in the pituitary cells of goldfish. These D1-binding sites were found to be saturable, stereospecific, and selective for D1 ligands. The rank order of binding affinity of these D1-binding sites is (+)SCH23390 > SKF83566 > (-)SCH23390 > domperidone > LY171555 > serotonin. The association of these D1-binding sites with [3H]SCH23390, a D1-specific radioligand, was rapid, reversible, and exhibited a high binding affinity in the nanomolar range. The Kd values were estimated to be 33.7 +/- 8.5 nM for mixed populations of pituitary cells and 10.9 +/- 2.5 nM for pituitary cell preparations enriched with somatotrophs. Autoradiographic studies revealed that specific binding of [3H]SCH23390 was predominantly localized in the pars distalis, not in the neurointermediate lobe of the goldfish pituitary. Furthermore, these D1-binding sites in the goldfish pituitary cells could be functionally correlated with the GH-releasing actions of DA. Since these D1-binding sites exhibited the expected pharmacological properties of mammalian D1 receptors, we conclude that DA D1 receptors are present in the goldfish pituitary and are responsible for the mediation of DA D1-stimulated GH release. The apparent similarities of the D1 receptor pharmacology between goldfish and mammals also suggests that DA D1 receptors are highly conserved during vertebrate evolution.

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Over 30 published papers, EMA documents and other information sources were collated, including two studies that met thorough QT study (TQT) criteria (ICH-E14). The first TQT1 was negative while the second was marginally positive. Reports of QT prolongation, ventricular arrhythmias and SCD were located (predominantly high/very high-dose IV domperidone). With oral domperidone, a Dutch case-controlled study reported an adjusted odds ratio of SCD of 11.4 (95% CI 1.99-65.2), based on only three patients out of 1,366 cases of SCD. A second nested case-controlled study calculated an odds ratio of ventricular arrhythmia or SCD of 1.59 (1.28-1.98) vs. placebo.