摘要
AIM:Toassessthemechanismsofprotectiveactionbydifferentmildirritantsthroughmaintenanceofgastricmucosalintegrityandmodulationofmucosalnitricoxide(NO)inexperimentalgastritisrats.METHODS:Etcher200mL/Lethanol,50g/LNaGor0.3mol/LHClwaspretreatedtonormalor800mL/Lethanol-inducedacutegastritisSprague-Dawleyratsbeforeasubsequentchallengewith500mL/Lethanol.Bothmacroscopiclesionareasandhistologicaldamagescoresweredeterminedinthegastricmucosaofeachgroupofanimals.Besides,gastricmucosalactivitiesofNOsynthaseisoformsandofsuperoxidedismutase,alongwithmucosallevelofleukotriene(LT)C4weremeasured.RESULTS:Macroscopicmucosaldamageswereprotectedby200mL/Lethanoland50g/LNaCIingastritisrats.However,although200mL/Lethanolcouldprotectthesurfacelayersofmucosalcellsinnormalanimals(protectionattenuatedbyNG-nitro-L-argininemethylester),nocytoprotectionagainstdeeperhistologicaldamageswasfoundingastritisrats.Besides,inducibleNOsynthaseactivitywasincreasedinthemucosaofgastritisanimalsandunalteredbymildirritants.Nevertheless,theelevationinmucosalLTC4levelfollowing500mL/Lethanoladministrationandundergastritisconditionwassignificantlyreducedbypretreatmentofallthreemildirritantsinbothnormalandgastritisanimals.CONCLUSION:Thesefindingssuggestthattheaggravated500mL/Lethanol-evokedmucosaldamagesundergastritisconditioncouldbeduetoincreasedinducibleNOandLTC4productioninthegastricmucosa.Only200mL/Lethanolistruly'cytoprotective'atthesurfaceglandularlevelofnongastritismucosa.Furthermore,themacroscopicprotectionofthethreemildirritantsinvolvesreductionofLTC4levelinbothnormalandgastritismucosa,implicatingpreservationofthevasculature.
出版日期
2004年12月22日（中国期刊网平台首次上网日期，不代表论文的发表时间）
