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The efficacy and safety of intravenous metoclopramide administered prophylactically before elective cesarean delivery under spinal anesthesia was studied.
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The author discusses the 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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As with colonoscopy, adequate bowel cleansing is essential prior to colon capsule endoscopy (CCE). Because CCE requires that the capsule traverse the entire gastrointestinal tract during the examination, laxative 'boosters' are used. The objective of this prospective, single-center, single-arm study was to evaluate the safety of a bowel preparation consisting of polyethylene glycol (PEG) plus an oral sulfate solution.
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In this report, we will describe the results of a cross-sectional study to assess PRL and GH secretion during the early follicular phase in 22 fertile patients after metoclopramide administration in order to achieve a dopaminergic DA2 receptor blockade. Blood samples were collected at - 15, 0, 15, 30, 45 and 60 minutes. PRL, GH, estradiol, IGF-I, TSH, glucose, and insulin were measured in the samples taken at - 15 and 0 minutes. The existence of a correlation between GH and PRL secretion was investigated. All patients presented normal serum levels of estradiol, prolactin, insulin, fasting glucose and IGF-I. Serum GH levels were not changed after metoclopramide infusion (p = 0.302), but there was a significant alteration in serum PRL (p = 0.0001) with the highest levels after 30 (mean: 237.20 ng/ml +/- 95.86) and 45 (mean: 211.80 ng/ml +/- 83.24) minutes. Serum GH levels did not correlate with serum PRL levels after the dopaminergic DA2 blockade. We conclude that GH secretion was not modulated by a direct effect of type 2 dopamine receptor.
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The aetiopathogenesis of ventilator-associated pneumonia (VAP) requires abnormal oropharyngeal and gastric colonization and the further aspiration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways, in whom mechanical, cellular and/or humoral defences are altered. Well-known risk factors for gastric colonization include: alterations in gastric juice secretion; alkalinization of gastric contents; administration of enteral nutrition; and the presence of bilirubin. However, the role of the colonized gastric reservoir in the development of VAP remains debatable. Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, controlled trials of selective gut decontamination and stress ulcer prophylaxis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respiratory infections. However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ventilation. Prophylactic measures suggested to prevent VAP in relation to the gastric reservoir include: treatment for stress ulcers with sucralfate; prevention of duodenal reflux with metoclopramide; reduction of gastric burden and bacterial translocation by selective digestive decontamination; acidification of enteral feeding; and jejunal feeding. Gastro-oesophageal reflux can be prevented by using small bore nasogastric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, checking the patency of the tube cuff, and aspiration of subglottic secretions. The role of the stomach as a reservoir for microorganisms causing ventilator-associated pneumonia is still controversial but despite the debate, there is major evidence in the literature in favour of the gastric origin of part of these pulmonary infections.
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This is the first prospective randomized study comparing commonly used antiemetics in children receiving cancer chemotherapy. We compared metoclopramide (MCP) with chlorpromazine (CLP), both administered in conventional doses, in 50 cancer patients aged 6 to 18 years who were receiving emetic chemotherapy. CLP proved significantly better than MCP in reducing both the frequency of vomiting (P less than .05) and the duration of nausea and vomiting (P less than .025). Extrapyramidal reactions (EPRs) were more common in MCP-treated patients. We conclude that, in the standard doses used, CLP is a better overall antiemetic than MCP for children receiving intensive chemotherapy. However, further prospective pediatric studies of antiemetic combinations are needed.
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In conclusion, the use of domperidone increases the CR of SBCE with PillCamSB. However, this increase does not translate into higher DY. A smart, tailored approach, which may include domperidone, purgatives, and real-time viewers, may be used in the clinical practice to improve DY until technology delivering capsules with much longer battery time becomes available.
The disposition of 4-amino-5-chloro-2-[2-(methylsulfinyl)ethoxy]-N- [2-(diethylamino)ethyl] benzamide hydrochloride (ML-1035) following intravenous (10 mg kg-1) and oral (200 mg kg-1) dosing was investigated in male and female New Zealand white rabbits. After intravenous dosing ML-1035 was eliminated with a half-life of 1.45 +/- 0.49 h in males and 0.79 +/- 0.08 h in females. Volume of distribution at steady-state was 2.08 +/- 0.98 l kg-1 in males and 9.11 +/- 5.86 l kg-1 in females. Clearance averaged 2.99 +/- 1.11 l h-1 kg-1 in males and 16.73 +/- 7.29 l h-1 kg-1 in females. All pharmacokinetic parameters were significantly different between males and females (p < 0.05). Absolute bioavailability after oral administration was 7.35 per cent for males and 12.31 per cent for females, suggesting that ML-1035 undergoes significant first-pass elimination. Plasma area under the curve for the metabolites of ML-1035 after both oral and intravenous administration were also different between the two sexes. These data suggest that the disposition of ML-1035 shows significant differences between male and female rabbits.
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Possible involvement of 5-hydroxytryptamine (5-HT), 5-HT receptors and prostaglandins in the acceleration of gastrointestinal transit by momordin Ic was investigated in mice. Accelerative effect of momordin Ic (25 mg/kg, p.o.) on gastrointestinal transit was attenuated by pretreatment with a bolus of DL-p-chlorophenylalanine methyl ester (an inhibitor of 5-HT synthesizing enzyme), but not repeated pretreatment with DL-p-chlorophenylalanine methyl ester. Furthermore, cyproheptadine (a nonselective 5-HT(2) receptor antagonist), ritanserin (a 5-HT(2A/2B/2C) receptor antagonist) and clozapine (a 5-HT(2A/2C) receptor antagonist) also attenuated the effect of momordin Ic, but methiothepin (a 5-HT(1) receptor antagonist), MDL 72222 (3-tropanyl-3,5-dichlorobenzoate) and metoclopramide (5-HT(3) receptor antagonists), tropisetron (a 5-HT(3/4) receptor antagonist), ketanserin and haloperidol (5-HT(2A) receptor antagonists) did not. These results suggested a possible involvement of endogenous 5-HT and 5-HT(2B/2C) over 5-HT(2A) receptors. Attenuation by pretreatment with indomethacin (an inhibitor of prostaglandins synthesis) suggested involvement of prostaglandins. It is postulated that momordin Ic accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT(2), possibly 5-HT(2C) and/or 5-HT(2B) receptors, which, in turn, increases synthesis of prostaglandins.
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The acute and chronic effects of metoclopramide on aldosterone secretion in the rat model were examined. Metoclopramide 50 micrograms iv in dexamethasone-treated rats did not increase plasma aldosterone concentration. Chronic infusion of metoclopramide (72 micrograms/hr) over 5 days also did not show any increase in the plasma or urinary aldosterone concentration when compared with control rats. Metoclopramide in vitro showed no effect on aldosterone secretion from rat adrenal capsular cells but it inhibited serotonin-mediated aldosterone secretion from the same cells significantly.