AIM:To assess the mechanisms of protective action bydifferent mild irritants through maintenance of gastricmucosal integrity and modulation of mucosal nitric oxide(NO)in experimental gastritis rats.METHODS:Either 200 mL/L ethanol,50 g/L NaCl or 0.3 mol/LHCl was pretreated to normal or 800 mL/L ethanol-inducedacute gastritis Sprague-Dawley rats before a subsequentchallenge with 500 mL/L ethanol.Both macroscopic lesionareas and histological damage scores were determined inthe gastric mucosa of each group of animals.Besides,gastric mucosal activities of NO synthase isoforms and ofsuperoxide dismutase,along with mucosal level of leukotriene(LT)C_4 were measured.RESULTS:Macroscopic mucosal damages were protectedby 200 mL/L ethanol and 50 g/L NaCl in gastritis rats.However,although 200 mL/L ethanol could protect thesurface layers of mucosal cells in normal animals(protectionattenuated by N~G-nitro-L-arginine methyl ester),nocytoprotection against deeper histological damages wasfound in gastritis rats.Besides,inducible NO synthase activitywas increased in the mucosa of gastritis animals andunaltered by mild irritants.Nevertheless,the elevation inmucosal LTC,level following 500 mL/L ethanol administrationand under gastritis condition was significantly reduced bypretreatment of all three mild irritants in both normal andgastritis animals.CONCLUSION:These findings suggest that the aggravated500 mL/L ethanol-evoked mucosal damages under gastritiscondition could be due to increased inducible NO and LTC_4production in the gastric mucosa.Only 200 mL/L ethanol istruly“cytoprotective”at the surface glandular level of non-gastritis mucosa.Furthermore,the macroscopic protectionof the three mild irritants involves reduction of LTC_4 levelin both normal and gastritis mucosa,implicating preservationof the vasculature. AIM: To assess the mechanisms of protective action by differen mild irritants through maintenance of gastric mucosal integrity and modulation of mucosal nitric oxide (NO) in experimental gastritis rats. METHODS: Either 200 mL / L ethanol, 50 g / L NaCl or 0.3 mol / LHCl was pretreated to normal or 800 mL / L ethanol-induced gastritis Sprague-Dawley rats before a subsequent challenge with 500 mL / L ethanol.Both macroscopic lesionareas and histological damage scores were determined in gastric mucosa of each group of animals. Besides, gastric mucosal activities of NO synthase isoforms and ofsuperoxide dismutase, along with mucosal level of leukotriene (LT) C_4 were measured.RESULTS: Macroscopic mucosal damages were protected by 200 mL / L ethanol and 50 g / L NaCl in gastritis rats. However, although 200 mL / L ethanol could protect the surface layers of mucosal cells in normal animals (protectionated by N ~ G-nitro-L-arginine methyl ester), nocytoprotection against deeper histological damages wasfound in gastr itis rats. Besides, inducible NO synthase activity was increased in the mucosa of gastritis animals andunaltered by mild irritants. Via, the elevation in mucosal LTC, level of 500 mL / L ethanol administration and under gastritis condition was significantly reduced by treatment of all three mild irritants in both normal andgastritis animals.CONCLUSION: These findings suggest that the aggravated 500 mL / L ethanol-evoked mucosal damages under gastritis condition could be due to increased inducible NO and LTC_4 production in the gastric mucosa. Only 200 mL / L ethanol istruly “cytoprotective” at the surface glandular level of non-gastritis mucosa.Furthermore, the macroscopic protection of the three mild irritants involves reduction of LTC_4 levelin both normal and gastritis mucosa, implicating preservation of the vasculature.