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  • 1
    ISSN: 1420-908X
    Keywords: Mild irritants ; Ethanol ; Gastric lesions ; Gastric emptying rate ; Mucosal folds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the involvement of gastric emptying and mucosal folds in the adaptive cytoprotection of different mild irritants against 100% ethanolinduced gastric mucosal damage. Pre-exposure to either 20% ethanol, 5% NaCl or 0.3M HCl significantly reduced the gastric mucosal damage caused by 100% ethanol in rats. Administration of either one of the three mild irritants increased the basal gastric residual volume and decreased the area occupied by gastric mucosal folds, but only 20% ethanol reduced the gastric emptying rate. Indomethacin (5 mg/kg, s.c.) pretreatment did not affect ethanol ulceration and gastric emptying rate when given by itself, but reversed the flattening of mucosal folds produced by the three mild irritants, and abolished the protective effect of 20% ethanol. These results suggest that the gastric adaptive cytoprotection induced by the three mild irritants acts through luminal dilution of the noxious agent, possibly caused by gastric retention. The reduction of mucosal folds could also contribute to the anti-lesion action of 20% ethanol. It is therefore suggested that the protective actions of the three mild irritants act through different mechanisms.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 11 (1997), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: The gastroprotective action of metronidazole, an antimicrobial used in the therapy against Helicobacter pylori infection, is unclear. Thus, the aim of the present investigation was to study the organoprotective action and antiulcer mechanisms of this drug in rodents. Methods and results: Metronidazole (10 mg/kg), given either per os or intraperitoneally, 30 min beforehand, reduced ethanol (40%, 10 mL/kg, p.o.)-induced gastric mucosal damage in male rats. Likewise, oral administration of metronidazole dose-dependently attenuated the indomethacin (30 mg/kg, p.o.)-induced gastric lesion formation and the concurrent depletion of mucosal mucus. However, metronidazole did not affect the basal mucosal prostaglandin E2 content. In an ex vivo gastric chamber preparation, 40% ethanol incubation markedly lowered transmucosal potential difference and increased mucosal vascular permeability in rat stomachs. Incubation with all doses of metronidazole did not modulate gastric mucosal blood flow nor transmucosal potential difference, either before or after ethanol treatment. Nevertheless, the increase in vascular permeability by 40% ethanol was significantly alleviated by either p.o. or i.p. metronidazole pre-treatment. In addition, exposure of the isolated rabbit gastric gland preparation to metronidazole (10−5 and 10−4 m) significantly attenuated the damaging action of 10% ethanol. Conclusion: It is concluded that metronidazole possesses a direct vascular and glandular organoprotective property in the rodent stomach. However, the anti-ulcer action does not appear to involve prostaglandins nor act through the improvement of gastric mucosal blood flow. Preservation of intramucosal mucus may partly contribute to the prevention of indomethacin-induced ulceration in rats.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of gastroenterology 30 (1995), S. 607-614 
    ISSN: 1435-5922
    Keywords: enprostil ; misoprostol ; duodenal ulcer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We conducted a clinical trial to compare the efficacy and safety profile of two prostaglandin analogues, enprostil (35 μg twice daily) and misoprostol (200 μg four times daily) in the treatment of acute duodenal ulcers in 214 patients. The two agents healed approximately 80% and in excess of 90% of duodenal ulcers after 4 and 6 weeks' therapy, respectively. There was a significantly lower ulcer healing rate in both treatment groups in smokers compared with nonsmokers (P〈0.05). However, daytime and nighttime ulcer pain relief was achieved in fewer than 50% of patients by either agent. Diarrhea, which occurred in more than 40% of patients, was the predominant side effect, and occurred mainly during the first 2 weeks of therapy with either agent. Nevertheless, this side effect was mild and self-limiting in the majority of patients. Both agents were found to be safe and well tolerated by the majority of patients. We conclude that these prostaglandin analogues are safe and effective duodenal ulcer healing agents. Furthermore, there was very little difference between enprostil and misoprostol. The limiting factors, however, for their routine use as ulcer healing agents are their low efficacy with regard to ulcer pain relief and the high incidence of diarrhea.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-2568
    Keywords: APOPTOSIS ; PROLIFERATION ; HELICOBACTER PYLORI ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; STOMACH
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It remains controversial whether the harmfuleffects of Helicobacter pylori (Hp) and nonsteroidalantiinflammatory drugs (NSAIDs) are additive. We studiedthe effects of Hp (virulent and nonvirulent strains) and NSAIDs, alone or in combination, onapoptosis and proliferation of gastric epithelial cellsin nonulcer dyspepsia (NUD) patients. Forty-four (25Hppositive and 19 Hp-negative) consecutive Chinese NUD patients with rheumatoid arthritis who hadtaken continuously NSAIDs for more than three monthswere recruited for this study. Another 41 (20Hp-positive and 21 Hp-negative) NUD patients not on anyNSAIDs were included as controls. All patientsunderwent a gastroscopy examination and gastricbiopsies. Hp infection was confirmed by CLOtest, anti-HpELISA, and [13C]urea breath test. The CagAstatus was determined by the anti-CagA antibody assay. The degree ofgastritis, apoptosis, and proliferation indices weredetermined with H&E staining, terminal uridinedeoxynucleotidyl nick end-labeling (TUNEL), andproliferating cell nuclear antigen (PCNA) immunostainingmethods, respectively. A significantly higher apoptosiswas observed in subjects who had Hp infection or hadbeen consuming NSAIDs when compared with the controls. Unlike NSAID-treated subjects, patients with Hpinfection were shown to have significantly enhanced cellproliferation. However, the increased apoptosis andproliferation in Hp-positive subjects were reversed by also taking NSAIDs. No correlation was foundbetween apoptosis and proliferation in all the studygroups. There was no association found between CagAexpression or degree of gastritis with cellproliferation or apoptosis. It was demonstrated at thecellular level that NSAIDs could abrogate apoptosis orproliferation effects induced by Hp. Furthermore, thelatter effects appeared not to be influenced by the virulent nature of the Hp strains.
    Type of Medium: Electronic Resource
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