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Based on data presented here, we concluded that diterpenoids and sterols detected in the ethanolic fraction can be responsible for its pharmacological activity.
Histamine (60 microM) produced ATP release from segments of guinea-pig vas deferens which was blocked by pyrilamine and triprolidine, H1-blockers, but not by ranitidine, an H2-blocker. The evoked-release was inhibited by the mitochondrial inhibitors, carbonyl cyanide-m-chlorophenylhydrazone (CCCP) and oligomycin. Bradykinin (BK) and substance P (SP) also caused substantial and moderate release of ATP, respectively. The BK-evoked release of ATP was inhibited by HOE140, a B2-antagonist, but not by [Des-Arg10] HOE140, a B1-antagonist. On the other hand, VIP, angiotensin II (AII) and cholecystokinin-octapeptide (CCK-8) failed to elicit a measurable release of ATP. Histamine and BK also enhanced the release of ATP from superfused cultured smooth muscle cells. These results suggest that ATP may be released as an autacoid from the smooth muscles in the presence of these chemical mediators.
To study in a double-blind controlled manner the effects of lansoprazole 15 mg or 30 mg daily compared with ranitidine 300 mg once daily and placebo in the relieving of symptoms and healing of acute duodenal ulceration.
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Patients were prospectively randomized to treatment with total parenteral nutrition, either alone, with sucralfate, or with ranitidine.
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JPHY could improve the proliferation of epithelial cells, inhibit gastric acid, improve microcirculation of gastric mucosa through the mediation of EGFR, so as to elevate the healing quality of gastric ulcer, display its anti-ulcer action.
A multicentre, parallel, randomized clinical trial.
Prospective, randomized, double-blind, parallel-group study in patients who were H. pylori positive on 13C urea breath test (13C UBT).
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Some additional omeprazole-related properties, such as antineutrophil properties, were not observed in H. pylori-infected mice after one week of treatment, suggesting that this property is restricted to in vitro approaches. However, the antiapoptotic activity of omeprazole could be attributed to an ability to modify the protein expression of Bcl-2, decreased by H. pylori infection.
The inhibitory effect of ranitidine and cimetidine on pentagastrin stimulated volume, acid and pepsin secretion has been studied in eight healthy volunteers. Both compounds inhibit all measured components of gastric secretion in a dose dependent manner. On a molar basis ranitidine is on average 11.14 times for volume, 13.04 times for acid, and 9.74 times for pepsin secretion more potent than cimetidine as measured by the ID50-values.
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As far as we know, this is the first case report of immediate hypersensitivity after Nd:YAG laser treatment of a tattoo. Prophylactic treatment with steroids and antihistamines prevented reactions with subsequent laser treatments. Reactions after laser removal are rare, but may increase as popularity of skin art increases with the need for subsequent removal.
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This prospective, single-center, randomized study included 464 consecutive Helicobacter pylori-positive patients with dyspeptic symptoms. A total of 415 patients completed the study. The patients were allocated into 4 study groups using random sampling numbers as follows-LAC group: lansoprazole 30 mg twice daily, amoxicillin 1000 mg twice daily, and clarithromycin 500 mg twice daily for 14 days; BLTM group: bismuth subcitrate 300 mg 4 times a day, lansoprazole 30 mg twice daily, tetracycline 500 mg 4 times a day, and metronidazole 500 mg twice daily for 10 days; RBLTM group: ranitidine bismuth citrate 400 mg twice daily, lansoprazole 30 mg twice daily, tetracycline 500 mg 4 times a day, and metronidazole 500 mg twice daily for 10 days; and LTM group: lansoprazole 30 mg twice daily, tetracycline 500 mg 4 times a day, and metronidazole 500 mg twice daily for 10 days.
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For maintenance treatment of reflux esophagitis, omeprazole alone or in combination with cisapride is more effective than ranitidine alone or cisapride alone, and the combination of omeprazole and cisapride is more effective than ranitidine plus cisapride.
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RBC and proton pump inhibitor have similar efficacy for H. pylori eradication when given with C and A for 1 week, but RBC seems to have a higher efficacy than proton pump inhibitor when C and N are the co-prescribed antibiotics.
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Smoking has been shown to impair the therapeutic effect of H2-receptor antagonists. To evaluate the acid-reducing capacity of H2-receptor antagonists in relation to smoking habits, we tested the effect of ranitidine (Ran) and famotidine (Fam) under physiologic conditions, using ambulatory pH-metry. Intragastric pH was measured over 20 h. Each of 18 healthy volunteers, 9 smokers and 9 nonsmokers, received 40 mg Fam, 300 mg Ran, or placebo in a double-blind, randomized study as a single evening dose. With both drugs 20-h acidity was markedly suppressed. After Fam treatment mean inhibition was 61% in smokers and 76% in nonsmokers and after Ran 51% and 67%, respectively. When areas under the pH curves for each individual were calculated and treatment compared with placebo (= 100%), the response was smaller in smokers than in nonsmokers with either drug (Fam, 153 +/- 21% versus 214 +/- 19%, p less than 0.01; Ran, 176 +/- 21% versus 232 +/- 29%, p less than 0.05) during the first 4 h after drug intake. A similar effect was observed in the morning period from 0600 to 1000 h (Fam, 118 +/- 19% versus 206 +/- 19%, p less than 0.001; Ran, 133 +/- 21% versus 207 +/- 31%, p less than 0.02). During the nighttime there were no significant differences. These findings indicate that smoking impairs the response to both drugs tested.
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The case of a patient with metastatic colorectal cancer who had a seizure during his intial cetuximab infusion is reported.
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In our study we found no difference between omeprazole and histamine H2 receptors antagonists in controlling and recurrence of upper gastrointestinal bleeding.
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36 patients with chronic gastric or oesophageal peptic ulceration (including 6 with antrectomy), resistant to high-dose ranitidine treatment for at least 3 months, were successfully treated with 40-60 mg of omeprazole daily for periods between 1 and 2 years. Fasting serum gastrin levels were monitored at regular intervals during therapy and multiple gastric mucosal biopsies were taken during gastroscopy every 3-6 months. Gastrin levels increased significantly during the first 6 months of therapy from a medium level of 81.5 to 206 pg/ml, a slight decrease was seen thereafter. In 10 patients investigated before the start of the treatment and after 1 and 2 years, the volume density of argyrophilic cells in the oxyntic mucosa increased from 0.43 +/- 0.08 to 0.91 +/- 0.14% during the first year; this change was statistically significant. No further increase was observed thereafter. No such difference could be demonstrated between a larger group of 18 patients investigated before and after 1 year of treatment with omeprazole (0.806 +/- 0.1 vs. 0.93 +/- 0.08%) and between a larger group of 22 untreated patients and 17 patients treated for 17-24 months with omeprazole (0.73 +/- 0.1 vs. 0.86 +/- 0.09%). The volume density of argyrophilic cells found in 8 patients with gastrinoma amounted to 1.37 +/- 0.22%. No clusters of endocrine cells were found in omeprazole-treated patients. The D cell volume density in the antral mucosa decreased significantly during the first months of treatment, but steadily increased thereafter to reach pretreatment values after 17 months. There was no change in G cell volume density under therapy. No changes in gastrin levels or oxyntic argyrophilic cells were observed in the antrectomized patients. It is concluded that the hyperplasia of argyrophilic cells observed in some patients during long-term omeprazole treatment is mediated by hypergastrinaemia.
A total of 22 subjects (13 with gastroesophageal reflux disease and nine who served as control subjects) were prospectively evaluated by serial combined esophageal and gastric 24-h pH monitoring. Studies were performed at baseline off antireflux medical therapy and subsequent to completion of the following four drug regimens: 1) omeprazole 20 mg b.i.d. for 2 wk; 2) omeprazole 20 mg b.i.d. plus ranitidine 300 mg HS for 4 wk; 3) omeprazole 20 mg QAM and QHS for 2 wk; and 4) omeprazole 20 mg every 8 h for 2 wk. A dual pH probe was placed 5 cm above and 10 cm below the manometrically defined LES for a minimum of 18 h. Median total, upright, and supine pH values were compared among treatment regimens. All subjects underwent Helicobacter pylori serology testing.
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Colonic carcinomas were induced in male Sprague-Dawley rats by six weekly intraperitoneal injections of methylazoxymethanol. Four weeks after the last injection of carcinogen, the animals were randomized into four treatment groups, including vehicle control, low- and high-dose omeprazole, and ranitidine. After 10 weeks of treatment, the animals were bled, stomach weights were recorded, and colon tumors were mapped, enumerated, measured, and scored histopathologically by Dukes' classification. Crypt and mucosal heights were determined in colonic mucosa unaffected by tumor.
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Nonsteroidal anti-inflammatory drugs induces gastric mucosal lesions because of its acidic properties. Ranitidine, an H2 receptor antagonist, has proved beneficial in patients with gastric ulcers.
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the incidence of IHNS was less than reported in the literature. The number of deaths associated with IHNS was low.
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Gastric and duodenal injury related to nonsteroidal anti-inflammatory drug (NSAID) use is extremely common, and a variety of strategies can be employed to reduce this frequent side effect of an otherwise useful category of medications. Although the best approach may be to discontinue NSAID treatment, this is not always possible for patients with arthritis pain or for those who require low-dose aspirin therapy for underlying cardiovascular disease. In arthritis cases, one of the new cyclooxygenase-2 specific inhibitors can be used to replace a traditional NSAID, but the addition of another drug to treat and heal ulcers is normally still needed. Patients taking aspirin are also candidates for additional treatment.
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A questionnaire was sent out in June 1998 to all French university hospital pharmacies and also to those public and private hospitals known to be involved in pediatric care. Of the 78 questionnaires mailed, 63 answers were received. The information requested concerned all the drug formulations prepared in 1997.
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Calotropis procera latex and flower extracts are toxic (50-70% mortality) even in a small dose (250 mg/kg) before washing off their toxic rubber. Zingiber officinale extract insignificantly decrease (7.26%) S. mansoni worms. When toxic rubber was washed off and ranitidine was used, C. procera (stem latex and flowers) and F. elastica extracts revealed significant S. mansoni worm reductions by 45.31, 53.7 and 16.71%, respectively. Moreover, C. procera extracts produced significant reductions in tissue egg load (∼34-38.5%) and positively affected oogram pattern.
A simple, selective and sensitive high-performance liquid chromatographic method with spectrophotometric detection was developed for the determination of antihyperglycemic agent metformin in human plasma using a novel sample extraction procedure. Liquid-liquid extraction of metformin and ranitidine (as internal standard) from plasma samples was performed with 1-butanol/n-hexane (50:50, v/v) in alkaline condition followed by back-extraction into diluted acetic acid. Chromatography was carried out using a silica column (250 mmx4.6 mm, 5 microm) under isocratic elution with acetonitrile-40 mM aqueous sodium dihydrogen phosphate (25:75, v/v), pH 6. The limit of quantification (LOQ) was 15.6 ng/ml and the calibration curves were linear up to 2000 ng/ml. The mean absolute recoveries for metformin and internal standard using the present extraction procedure were 98 and 95%, respectively. The intra- and inter-day coefficient of variation and percent error values of the assay method were all less than 8.3%.
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Adults with at least a 3-month history of heartburn were eligible for this randomized, double-blind, parallel group, multicentre dose-ranging study. Following a 1-week open-label run-in phase to document baseline heartburn frequency, subjects were randomized to receive treatment with one tablet of either ranitidine 75 mg (n = 491), ranitidine 25 mg (n = 504), or placebo (n = 494), to be taken as needed up to four times daily for 2 weeks for the relief of heartburn.
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Sucralfate (Sc) suspension 6 g/day and ranitidine (Rn) tablets, 150 mg, were compared in 125 patients in a double-blind, multicenter, endoscopically controlled trial in the treatment of reflux esophagitis. Inclusion criteria were symptomatic reflux (number and severity of attacks) and endoscopic evidence of esophagitis (grades 1 to 4). Clinical assessments were performed on entry, and at 4 and at 8 weeks, and endoscopy was repeated at 8 weeks. Sc suspension and Rn placebo or Sc placebo and Rn tablets were taken on waking and immediately before retiring at night. Of the 125 patients, 27 were withdrawn because of default (Rn = 4; Sc = 14), noncompliance (Rn = 1; Sc = 2), or the development of congestive cardiac failure (Rn = 1), diarrhea (Rn = 1; Sc = 1), nausea (Sc = 1), constipation (Sc = 1), and hematemesis (Sc = 1). Analysis was performed on the remaining 98 patients, 43 of whom had been treated with Sc and 55 with Rn. Heartburn, acid regurgitation, epigastric pain, dysphagia, and chest pain were relieved in 34% vs 40%, 67% vs 72%, 71% vs 57%, and 86% vs 63% for Sc and Rn, respectively. There was no significant difference between the two groups. Endoscopic healing occurred in 47% of the Sc- and in 31% of the Rn-treated patients (chi 2 = 2.50), and healing or improvement was noted in 81% of the Sc- and 64% of the Rn-treated patients. This difference approached statistical significance (chi 2 = 3.73). There was no obvious endoscopic benefit in 8 of the 43 and 20 of the 55 patients in the groups treated with Sc and Rn, respectively. Although the findings with sucralfate and ranitidine in patients with reflux esophagitis completing the trial suggest a benefit of these agents, the absence of a placebo control group and the high default rates, particularly for those receiving sucralfate, preclude any firm conclusions as to relative or specific efficacy of these agents in this condition.
1. Quinpirole did not produce any effect in isolated uterus from oestrogenized rats even when it is contracted by KCl (37 mM). 2. Fenoldopam produced a relaxant effect on rat isolated uterus contracted by KCl which was not significantly modified by SCH 23390. 3. Reserpine decreased the effect of the lowest doses of fenoldopam. In reserpinized rats, propranolol (10(-9), 10(-8), 10(-7) M) antagonized the effect of the lowest doses of fenoldopam and neither SCH 23390, sulpiride nor ranitidine modified the effect of fenoldopam. 4. The results confirm our previous finding that DA1-receptors are not functional in our preparation. The effect of fenoldopam was partially due to a catecholamine-releasing action.