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  • 1
    ISSN: 1420-908X
    Keywords: Adaptive cytoprotection ; Lesions ; Nonprotein sulfhydryl compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The contribution of the endogenous nonprotein sulfhydryl compounds (SH) in gastric adaptive cytoprotection was investigated in rats. N-ethylmaleimide (NEM) treatment significantly reduced mucosal SH level, and aggravated the mucosal injury induced by absolute ethanol. Oral administration of the mild irritants, 20% ethanol, 5% NaCl or 0.3 M HCl, significantly increased the basal mucosal SH level. These agents also showed a cytoprotective action against the necrotizing effect of absolute ethanol. Administration of NEM did not alleviate this cytoprotective potential, although it abolished the increased SH level evoked by these mild irritants. Thus, it is concluded that modulation of endogenous SH by mild irritants perhaps only plays a minor role in the gastric adaptive cytoprotection.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 48 (1999), S. 471-478 
    ISSN: 1420-908X
    Keywords: Key words: Nitric oxide — Prostaglandins — Adaptive cytoprotection — Ethanol — Gastric defense — Mucosa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: The correlation between mucosal generation of nitric oxide (NO) and prostaglandin E2 (PGE2) in gastric adaptive cytoprotection was investigated.¶Materials and Treatment: Male Sprague-Dawley rats were pretreated with either Nw-nitro-L-arginine methyl ester (L-NAME, 12.5mg/kg i.v.) or indomethacin (5mg/kg s.c.). Following that, mild irritant 20% ethanol was administered, 15min prior to 100% ethanol challenge.¶Methods: Macroscopic gastric mucosal damage, NO synthase activity, mucosal PGE2 and leukotriene C4 (LTC4) levels were measured.¶Results: Administration of L-NAME and indomethacin significantly reduced the protective action of 20% ethanol against 100% ethanol-induced gastric mucosal damage. Besides, mucosal activity of constitutive NO (cNO) synthase, but not of the inducible isozyme (iNO synthase), was elevated following 20% ethanol treatment. This was accompanied by a reduction in mucosal leukotriene C4 level. Indomethacin significantly inhibited mucosal PGE2 biosynthesis but increased cNO synthase activity. Nevertheless, L-NAME reduced both cNO and iNO formation and prevented the increase in cNO formation caused by 20% ethanol, while enhancing mucosal PGE2 production. Combined L-NAME and indomethacin treatment markedly potentiated ethanol-induced mucosal damage, and completely prevented the increase in cNO or PGE2 biosynthesis when either compound was given alone.¶Conclusions: These findings suggest a co-regulatory relationship between mucosal NO and PG in the gastric defense system, which will be released after activation by the mild irritants to induce cytoprotection.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 40 (1995), S. 2312-2316 
    ISSN: 1573-2568
    Keywords: dorsal motor nucleus of vagus ; ethanol ; gastric mucosal blood flow ; gastric acid secretion ; gastric damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Experimental evidence indicates that the autonomic nervous system, especially the cholinergic pathway, modulates the mucosal defensive mechanism and affects mucosal damage in the stomach. The present study investigated the role of the dorsal motor nucleus of vagus (DMV) in gastric function and its influences on ethanol-induced mucosal damage in pentobarbitone-anesthetized rats. Electrolytic lesion of the DMV as compared with sham operation and lesions of other brain areas, eg, nucleus reticular gigantocellularis and cuneate nucleus, reduced the basal gastric mucosal blood flow (GMBF) and also the blood flow after ethanol administration. The same operation did not affect the acid secretion either in the basal state or during the ethanol treatment period. Lesions at the caudal half of the DMV produced a bigger depression of GMBF when compared with lesion at the rostral half. In the sham-operated rats, ethanol induced severe hemorrhagic lesions in the gastric glandular mucosa, and this was significantly potentiated by lesions at the DMV, especially in the caudal half. The present findings indicate that acute DMV damage at the caudal half markedly affects the GMBF but not the acid secretion. The action on GMBF may contribute to the aggravation of ethanol-induced gastric damage in rats. These data reinforce the idea that the central vagal pathway, especially the caudal half of the DMV, plays a significant role in the modulation of GMBF, which in turn affects the integrity of gastric mucosal barrier.
    Type of Medium: Electronic Resource
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