简介：Objective:Impairedactivefluidtransportofalveolarepitheliummayinvolveinthepathogenesisandresolutionofalveolaredema.Thcobjectiveofthisstudywastoexplorethechangesinalveolarepithelialliquidclearanceduringlungedemafollowingacutelunginjuryinducedbyoleicacid.Methods:Forty-eightWistarratswererandomlydividedintosixgroups,I.e.,injured,amiloride,ouabain,amilorideplusouabainandterbutalinegroups.Twenty-fourhoursaftertheinductionofacutelunginjurybyintravenousoleicacid(0.25ml/kg),5％albuminsolutionwith1.5μCi125Ⅰ-labeledalbumin(5ml/kg)wasdeliveredintobothlungsviatrachea.Alveolarliquidclearance(ALC),extravascularlungwater(EVLW)contentandarterialbloodgasesweremeasuredonehourthereafter.Results:At24haftertheinfusionofoleicacid,theratsdevelopedpulmonaryedemaandseverehypoxemia,withEVLWincreasedby47.9％andALCdecreasedby49.2％.Additionofeither2×10-3Mamilorideor5×10-4MouabaintotheinstillationfurtherreducedALCandincreasedEVLW.ALCincreasedbyapproximately63.7％andEVLWdecreasedby46.9％withimprovedhypoxemiaintheTerbutaline(10-4M)group,comparedthoseininjuredrats.AsignificantnegativecorrelationwasfoundbetweentheincrementofEVLWandthereductionofALC.Onclusions:Activefluidtransportofalveolarepitheliummightplayaroleinthepathogenesisoflungedemainacutelunginjury.