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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.

Other names for this medication:

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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 25-yr-old man suffered from severe nocturnal asthma, which was shown to be provoked by pathological gastro-oesophageal reflux. A dramatic, immediate improvement of his pulmonary condition was achieved by treatment with omeprazole after failure of other therapeutic measures, including high doses of ranitidine.

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An electrophysiological study was performed to elucidate the role of nicotinic receptors in the striatal neurons in chloral hydrate-anesthetized rats. The effects of microiontophoretic application of nicotine and other drugs were examined on the caudate nucleus (CN) neurons activated monosynaptically by stimulation of the substantia nigra pars compacta (SN). Application of nicotine facilitated spontaneous firing. The nicotine-induced firing of the CN neurons was inhibited by concomitant application of domperidone or hexamethonium. These findings suggested that nicotine enhances dopamine release from the SN-derived dopaminergic nerve terminals by activating the neurons via D2 receptors.

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This study was conducted to identify the vascular dopamine receptor subtype responsible for specific dopamine-mediated coronary vasodilation. The left circumflex coronary artery (LCX) of pentobarbital anesthetized, open chest dogs was isolated and perfused under either constant flow or constant pressure conditions with blood withdrawn from a cannulated left femoral artery. In animals subjected to constant flow LCX perfusion, after beta adrenoceptor blockade with nadolol (4 mg/kg), alpha-1 adrenoceptor blockade with prazosin (0.5 mg/kg) and alpha-2 adrenoceptor blockade with idazoxan (1.0 mg/kg), intracoronary (c) injection of dopamine (0.01-10 micrograms/kg) produced a dose-dependent decrease in LCX perfusion pressure which was unaltered by administration of the dopamine-2 receptor antagonist domperidone (10 micrograms/kg) but which was blocked completely by the dopamine-1 receptor antagonist SK&F R-83566 (5 micrograms/kg). Similarly, under conditions of constant pressure LCX perfusion and after combined beta, alpha-1 and alpha-2 adrenoceptor blockade, i.c. administration of dopamine produced a dose-related increase in LCX coronary blood flow which was inhibited by SK&F R-83566 but not by domperidone. Direct i.c. administration of the selective dopamine-1 receptor agonist, fenoldopam (1 microgram/kg), resulted in an increase in LCX coronary blood flow which was eliminated completely after administration of SK&F R-83566. Doses of the selective dopamine-2 receptor agonist, dipropyldopamine (0.1-30 micrograms/kg), effective in producing blood flow increases in the femoral vascular bed and which could be antagonized by domperidone, produced only minimal and inconsistent changes in LCX coronary blood flow. Our data demonstrate that direct, dopamine-mediated coronary vasodilation in vivo occurs via stimulation of a vascular receptor of the dopamine-1 subtype.

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Milk leakage from the breast, which is known as galactorrhea, can be caused by a number of pharmacological, physical, and tumoral factors. Galactorrhea is a well-known side effect of domperidone, and is usually associated with hyperprolactinemia. However, euprolactinemic galactorrhea secondary to domperidone is very rarely seen and has yet to be reported in children before. Here, we report an adolescent with euprolactinemic galactorrhea caused by domperidone.

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Dopaminergic stimulation by apomorphine causes severe adverse effects such as vomiting and sedation. We compared the effectiveness of the serotonin 5-HT(3) antagonistic antiemetic drug ondansetron in a single oral dose with the standard regimen using domperidone TID 2 days prior to stimulation. In a double blind, randomised parallel group design, 16 previously untreated Parkinsonian patients were investigated, eight patients received domperidone (total dose 140 mg, starting 2 days prior to apomorphine challenge) and eight patients ondansetron (8 mg single dose 2 hr prior to investigation). Adverse events following the injection of 2-3 mg apomorphine were rated on a four-item scale. In an overall analysis, dopaminergic stimulation was significantly better tolerated, if the patients received domperidone, whereas more severe adverse effects were noted after ondansetron. Following ondansetron pre-treatment, seven patients experienced marked nausea or vomiting, all patients yawned, six patients had marked sedation, two patients a blood pressure decrease of more than 20 mmHg, and four patients strong sweating. In contrast, the latter side effect was found only in one patient pre-treated with domperidone, no patient had significant blood pressure decrease, all patients yawned, and seven domperidone patients had slight nausea. We conclude that oral ondansetron is no alternative to domperidone in the pre-treatment regimen of dopaminergic stimulation.

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There is little information concerning the long term outcome of patients with gastro-oesophageal reflux disease (GORD). Thus 109 patients with reflux symptoms (33 with erosive oesophagitis) with a diagnosis of GORD after clinical evaluation and oesophageal testing were studied. All patients were treated with a stepwise approach: (a) lifestyle changes were suggested aimed at reducing reflux and antacids and the prokinetic agent domperidone were prescribed; (b) H2 blockers were added after two months when symptoms persisted; (c) anti-reflux surgery was indicated when there was no response to (b). Treatment was adjusted to maintain clinical remission during follow up. Long term treatment need was defined as minor when conservative measures sufficed for proper control, and as major if daily H2 blockers or surgery were required. The results showed that one third of the patients each had initial therapeutic need (a), (b), and (c). Of 103 patients available for follow up at three years and 89 at six years, respective therapeutic needs were minor in 52% and 55% and major in 48% and 45%. Eighty per cent of patients in (a), 67% in (b), and 17% in (c) required only conservative measures at six years. A decreasing lower oesophageal sphincter pressure (p < 0.001), radiological reflux (p = 0.028), and erosive oesophagitis (p = 0.031), but not initial clinical scores, were independent predictors of major therapeutic need as shown by multivariate analysis. The long term outcome of GORD is better than previously perceived.

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The effect of domperidone, a peripheral dopamine receptor antagonist, has been studied in the aspirin, phenylbutazone and reserpine induced gastric ulcers in rats. The gastric anti-ulcer activity of domperidone was evident following a single dose as well as a 5-day pretreatment against all the three ulcerogenic drugs. However, the protection in the five-day pretreatment group was greater than in the single dose pretreatment group. It appears that the gastrokinetic properties of domperidone play a significant role in producing this anti-ulcer effect. The study substantiates the results of the clinical observations on the healing of gastric ulcers and provides a rationale for further clinical studies in that direction. The possible mechanisms of action of this agent are discussed.

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This study was aimed at in vivo characterisation of the possible role of dopamine receptors in the modulation of adrenaline release from the adrenal medulla in rats. Quinpirole (0.3, 1 and 3 mg/kg s.c., 30 min), an agonist at dopamine D2-like receptors induced a statistically significant increase not only in adrenal dopamine but also in plasma and heart adrenaline levels. The effects of the lowest dose of quinpirole were blocked by domperidone (5 mg/kg s.c., 150 min). Implantation of catheters followed by blood sampling appeared to be a stressful procedure, inducing itself an elevation of adrenal dopamine and of heart adrenaline by 100 and 250%, respectively. To explore the possibility of determining the plasma levels of adrenaline without blood sampling, regression modelling was performed by means of partial least squares regression (PLS) using treatment and levels of heart adrenaline and adrenal dopamine as predictor variables. The selected variables were found to be good predictors of plasma adrenaline levels. Accordingly, the increase in adrenal dopamine and heart adrenaline levels following administration of the dopamine autoreceptor agonist, talipexole, and the classical non-selective dopamine receptor agonist, apomorphine, were interpreted as indicators of the increased adrenomedullary adrenaline release. Neither of the dopamine D2 receptor antagonists used, i.e. domperidone, supposed to have only peripheral effects, nor raclopride, had significant effects on adrenal dopamine and heart adrenaline. Our results support the presence of peripherally located dopamine D2-like receptors, capable of acutely stimulating not only the synthesis of catecholamines, but also the release of adrenaline from adrenals in the conscious rat.

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Accurate, selective and sensitive spectrophotometric methods have been developed and validated for simultaneous determination of Cinnarizine and Domperidone, a binary mixture with overlapping spectra, without preliminary separation. These methods include area under the curve (AUC) and dual wavelength spectrophotometry. For the AUC method, the area under curve of mixture solutions in the wavelength ranges 241-258 nm and 280-292 nm were selected for determination of Cinnarizine and Domperidone and by applying Cramer's rule, concentration of each drug was obtained. In dual wavelength method, two wavelengths were selected for each drug in a way so that the difference in absorbance is zero for another drug. Domperidone shows equal absorbance at 240.2 nm and 273.2 nm, where the differences in absorbance were measured for the determination of Cinnarizine. Similarly, differences in absorbance at 230.8 nm and 259.2 nm were measured for determination of Domperidone. The proposed methods were applied for determination of Cinnarizine and Domperidone over the concentration ranges of 2-20 and 2-22 μg mL(-1), respectively. The suggested methods were validated as per USP guidelines and the results revealed that they are reliable, reproducible and precise for routine use with short analysis time. The results obtained by the proposed methods were statistically compared to the reported method, and there was no significant difference between them regarding both accuracy and precision.

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All studies including humans and published in English with data assessing the efficacy of galactogogues for increasing breast milk production were evaluated.

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The objective of this study was to evaluate the practice among Japanese physicians of the prophylactic use of antiemetics when starting opioids prescription for the prevention of opioid-induced nausea and vomiting.

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We identified putative occurrences of hospitalization for SD/VA in patients receiving outpatient prescriptions for cisapride, domperidone, or metoclopramide. We then administered a questionnaire to Cialis Cost Walmart general practitioners (GPs) caring for these patients, requested hospital discharge consult letters, and examined the positive predictive value (PPV) of diagnostic codes in identifying outpatient events precipitating hospitalization.

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Among 120 patients 113 patients completed this study in three groups (G-1 Levosulpiride 40 patients, G-2 Domperidone Simvastatin Zocor Generic 35 patients and G-3 Metoclopramide 38 patients) were followed up. Female gender was dominated (75), occupation wise most of patients belong to laborer (49) class. Highly significant improvement in symptoms scale was noticed in G-1 Levosulpiride 40 patients' group.

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Selective UGE is cheaper and appears not to compromise the response to prokinetics; however, its diagnostic power is less than with Cheap Cymbalta Canada mandatory UGE.

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After reviewing the pharmacologic properties of apomorphine, the English language literature is summarized with particular attention on articles resulting from a Medline search of apomorphine and Parkinson Avapro Generic Picture disease limited to randomized controlled studies. Other formulations and indications for treatment of movement disorders are also discussed.

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This randomized, double-blind, double-dummy, positive-controlled study compared the efficacy and safety of cinitapride (1 mg) and domperidone (10 mg) tid for 4 weeks in 383 consecutive patients with mild to moderate, postprandial distress syndrome-predominant dyspeptic symptoms according to Rome III criteria. The primary endpoint was the noninferiority of cinitapride compared with domperidone in relief of symptoms. The overall patient evaluation of Flonase Generic Costco treatment and open gastric emptying effects of both drugs were treated as the secondary endpoints.

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MCG containing DM was prepared by screening different concentrations of sweeteners, flavouring agents, softening Zofran Generic agents, lubricants and anti-adherents by changing one variable at a time. Performance evaluation was carried out by evaluating size, shape, thickness, taste, scanning electron microscopy, texture analysis, in vivo drug release study, ex vivo buccal permeation study and by studying statistical analysis for quality.

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To verify if the low estrogen regimen could condition the TSH hyperresponsivity and PRL hyporesponsivity to antidopaminergic drugs seen by us and others in patients bearing prolactinoma, the effect of ethynilestradiol treatment (50 micrograms/day/14 days) on TSH and PRL responses to domperidone in 6 women with tumoral hyperprolactinemia and hypoestrogenemia were studied. Estrogenic treatment was unable to modify the TSH and PRL responsiveness either to domperidone and TRH. These data do not support the hypothesis that hypoestrogenemia could cause the peculiar TSH and PRL pattern in response to antidopaminergic drugs, in patients bearing prolactinoma. Also the TRH releasable pool Proscar Cost Ireland of TSH and PRL in these patients seems to be unaffected by estrogenic treatment.

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In the open-label trial, 493 of 772 evaluable subject-nights were free of snoring; another 232 nights were scored as mild snoring. In the placebo-controlled trials, low-dose therapy caused a reduction in snoring, and high-dose therapy even a greater reduction in snoring. The Benicar Online drug combination was more effective than either agent alone.

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The possible involvement of the dopaminergic system in the serotonin (5-HT)-stimulated prolactin (PRL) secretion was tested in this study. Adult female rats were ovariectomized for two weeks and treated with estrogen (polyestradiol phosphate, 0.1 mg/rat, sc) for 6 days before use. They either received pretreatment with alpha-methyl-p-tyrosine (250 mg/kg BW, ip), a dopamine (DA) synthesis inhibitor, or two DA antagonists, domperidone and haloperidol (0.1 mg/kg BW, iv) before receiving 5-HT (1 mg/kg BW, iv) or quipazine (1 mg/kg BW, iv), a 5-HT agonist. Blockade of DA synthesis or antagonism of DA action invariably induced elevated plasma PRL levels. 5-HT or quipazine, however, could still induce significant PRL secretion on top of the increased PRL Nizoral Tablets Buy levels. Minor difference was found between the action of domperidone and that of haloperidol. In conclusion, the dopaminergic system may not be involved in the action of 5-HT to stimulate PRL secretion.

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Both acute and chronic oral administration (1-20 mg/kg) of FCE 22716, a new ergoline derivative, resulted in a dose-related fall of arterial blood pressure lasting for more than 6 h. Tachycardia was observed only at high dosages. Yohimbine, propranolol and indometacin did not modify its antihypertensive effect; on the other hand pretreatment with prazosin, a selective alpha 1-adrenoceptor antagonist and pithing, almost completely neutralized its antihypertensive effect. Haloperidol, a dopamine antagonist that crosses the blood-brain barrier, also antagonized FCE 22716 activity. The lack of effects of domperidone (DA2-receptor antagonist selectively acting on the periphery) together with the finding that norepinephrine and epinephrine levels were unchanged after treatment with FCE 22716, seem to rule out an involvement of peripheral DA2-receptors. Both in vitro (isolated organs) and in vivo the compound antagonized responses mediated by stimulation of alpha 1-adrenoceptors and S2-receptors. Radioligand binding studies in different cerebral regions are in line with the above reported in vitro and in vivo results. These data suggest that FCE Crestor Go Generic 22716 is endowed with a multitarget mechanism of action, mainly involving blockade of alpha 1-adrenoceptors and S2-receptors.

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It is note that hyperprolactinemia is frequently associated to chronic renal failure (CRF). The etiopathogenesis of this endocrine disorder is not clearly understood, trying to evaluate the possible hypothalamic-pituitary cause we have evaluated the Prl levels under some pharmacological tests: TRH (200 mcg i.v.),Domperidone (DOM)(10 mg i.v.),Nomifensine (NOM)(200 mg p.o.)and Bromocriptine (BRC)(2.5 mg p.o.) in 3 groups of patients: CRF(8 cases), dysfunctional (8 cases) and tumoral (9 cases) hyperPrl. Prl plasma levels have been evaluated by RIA (kits,Biodata,Roma). In patients affected by CRF either direct (BRC) than indirect (NOM) agonist acting dopaminergic drugs failed to induce a reduction in Prl plasma levels, like to tumoral patients for NOM, and in contrast to the significant decrease after BRC (-70%) in tumoral and (-74%) in dysfunctional and NOM (-50%) observed in dysfunctional patients. CRF and dysfunctional patients showed significant response to TRH and DOM, being prolactinoma bearing patients unresponsive to these tests. These results show an hyporesponsivity of pituitary Prl secreting cells to dopaminergic control suggesting the existence of central etiopathological factor in inducing hyperprolactinemia in CRF patients.

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Dogs exposed to 8 Gy 60Co gamma mid-abdominal irradiation exhibited emesis with an average latency of 102 min and an average of 7.4 episodes over 96 min. There were no significant changes in dogs subjected to a chronic bilateral subdiaphragmatic vagotomy, but emesis was prevented by ablation of the area postrema. Indomethacin pretreatment also prevented radiation-induced emesis in two of seven dogs and in the remainder reduced the average number of episodes. Domperidone pretreatment prevented radiation-induced emesis in all of four dogs tested. In electrophysiological studies recording from the area postrema the chemosensitive neurons were found to be normally silent in anesthetized preparations but excitable by a variety of emetic agents. After irradiation of the abdomen spontaneously active neurons were found with a discharge pattern that mirrored the behavioral pattern of postirradiation emesis. These studies are consistent with radiation-induced emesis being humorally mediated in the dog and implicate dopamine and/or prostaglandins as possible mediators.