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Ten groups of rats were used and orally administered 10% DMSO (negative control), 100 mg/kg ranitidine (positive control) or MEMM (50, 250 and 500 mg/kg) followed by gastric ulcer induction either using ethanol or indomethacin. The stomachs were collected and subjected to macroscopic and microscopic analyses.
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The H2-blockers, cimetidine and ranitidine, are reported to inhibit liver regeneration. In this work, the effects of a new powerful H2-receptor antagonist, famotidine, on liver regeneration were studied in rats. The animals were divided into three groups: group I in which a standard two-thirds hepatectomy was performed, group II in which the rats were treated with famotidine (intramuscular dose of 0.8 mg/kg body weight) on the day of operation and 24 and 48 h after hepatectomy, and group III in which the animals were intramuscularly injected with a larger dose of famotidine (1.2 mg/kg body weight) in the same way as group II. The histology and mitotic index of remnant livers and serum levels of aminotransferase and albumin were examined from 24 h to 10 days after the operation. The treatment with famotidine (groups II and III) did not inhibit hepatocyte mitosis but, on the contrary, raised the index on day 3 after hepatectomy when compared with the controls (group I). The albumin synthesis was well preserved in the famotidine-treated animals. The noninhibitory effects of famotidine on liver regeneration are discussed.
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The cardiothoracic surgery database at our institution was used to identify retrospectively all patients who had received SUP with pantoprazole or ranitidine, without crossover between agents. From January 1, 2004, to March 31, 2007, 887 patients were identified, with 53 patients excluded (pantoprazole, 30 patients; ranitidine, 23 patients). Our analysis compared the incidence of nosocomial pneumonia in 377 patients who received pantoprazole with 457 patients who received ranitidine.
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Four weeks of lansoprazole (30 mg daily) or ranitidine (300 mg daily) therapy produced a significant decrease in H. pylori infection. The reduction of H. pylori infection, but not ulcer healing per se, correlated with the decrease in active and chronic antral inflammation. Reduction of H. pylori infection, however, did not improve the good ulcer-healing rates already achieved at 4 wk by potent acid inhibition.
The gastric pH and volume were measured in 175 patients undergoing elective, and 313 undergoing emergency, obstetric procedures. Ranitidine 150 mg was administered orally every 6 hours in labour and at least 2 hours before elective Caesarean section. Patients received 20 ml of 8.4% sodium bicarbonate orally immediately prior to induction of anaesthesia. The combination of ranitidine and sodium bicarbonate produced marked alkalinisation of gastric contents (mean pH 8.9). The administration of sodium bicarbonate pre-operatively in patients who received ranitidine less than 2 hours before operation led to satisfactory elevation of gastric pH. Only four patients had a gastric pH less than 2.5, one patient refused any medication, two received only ranitidine and one patient had a long interval from administration of bicarbonate to aspiration of gastric contents. Gastric volumes were high in labouring patients (mean 84 ml) despite administration of ranitidine. The effectiveness of sodium bicarbonate as a single dose antacid therapy prior to obstetric anaesthesia requires further study.
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Prospective randomized controlled trial.
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The four children were 6.9-11.3 years old and weighed 20.4-49.5 kg. The Low Doses were 1.5-2.7 mg/kg; the High Doses were 3-5 mg/kg. Although the mean percentage of time with gastric pH > 4 during the entire 6 hours following dosing was similar after Low and High Dose (50% vs. 57%, NS), during the last two hours of this interval the mean percentage of time with gastric pH > 4 was only 29% for Low Dose vs. 89% for High Dose (P = 0.006). Moreover, during those two hours, none of the Low Doses kept gastric pH above 4 for > 60% of the time, while all of the High Doses kept pH above 4 for > 60% of the time (P = 0.03). In three of four patients who underwent extended (9-12 h) gastric pH monitoring after High Dose ranitidine, gastric pH was above 4 for more than 40% of total time.
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Candida overgrowth in gastric juice of peptic ulcer subjects under therapy with H2-receptor (H2-R) antagonists has been detected in 21.4 and 53.8% of cases after short- and long-term treatment respectively, and in 8% of controls. Both types of H2-R antagonists, ranitidine and cimetidine, were equally associated with production of yeasts. The location of ulcers, whether gastric or duodenal, seems to have no influence on fungal growth. Females were more susceptible than males to develop Candida in gastric juice. In the short-term course with H2-R blockers fungal colonization of gastric juice was associated with delay of the rate of ulcer healing. Fungal detection in gastric juice was not associated with mucosal invasion by Candida since in none of the patients who had a biopsy for gastric ulcer was Candida detected by histology.
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We studied whether a single oral dose of either cimetidine or ranitidine affects the disposition of epidurally administered lidocaine in the parturient. Patients given epidural analgesia for elective caesarean section were randomly pretreated with either cimetidine 400 mg (n = 5), ranitidine 150 mg (n = 7) or no H2 receptor antagonist (n = 5). Following the administration of 400 mg of lidocaine 2% with adrenaline 1:200,000 no difference was found in peak plasma lidocaine levels or area under the plasma concentration/time curve (AUC) between the three groups. A single oral dose of cimetidine or ranitidine does not affect lidocaine disposition in the obstetric patient.
Ranitidine was useful and could significantly reduce the harmful gastric effects of antiblastic drugs, as has been extensively shown by the literature. These drugs can lead to the suspension of treatment owing to intolerance or even death. In this study ranitidine reduced the damaging effects on the upper digestive tract in respectively 78% of the cases treated compared to 22% of non-responders.