ObjectiveToestablishananimalmodelofsuddenonsetsensorineuralhearingloss(SSNHL)tostudyitsmechanisms.MaterialsandmethodsTheinnerearwasexposedto3-nitropropionicacidat0.5mol/L(3-NP(H))and0.3mol/L(3-NP(L))throughtheroundwindowmembranefor30minutesin50maleguineapigs.Thresholdsofauditorybrainstemresponses(ABR)wereestablishedbeforethetreatmentandretestedat4hours,1day,3daysand6daysfollowing3-NPexposure.Controlanimalsweretreatedwithphosphatebufferedsaline(PBS)andtheirABRswereretestedat4hoursand1dayafterthetreatment.Animalsweremonitoredfornystagmusandposturalsignsofvestibulardysfunction,usingadigitalvideocamera,followingthetreatmentprocedure.Specimensweretakenat12hours,1day,3daysand7daysfollowing3-NP(H)exposureandembeddedinJB4forlightmicroscopyobservation.ResultsABRswerelostinallanimalstestedat4hoursfollowing3-NP(H)exposure.TherateofcompleteABRlossdecreasedaspost-treatmenttesttimeincreased.ABRswerelostin80%(4/5)oftheanimalsat1dayafterexposureto3-NP(L).Spontaneoushorizontalnystagmuswithafastphaseawayfromthetreatedeardevelopedinall3-NP(H)-treatedanimalsandin20%(1/5)oftheanimalsexposedto3-NP(L),exceptfortheonetreatedbilaterally.Variousdegreeofposturaldisturbancesconsistentwithunilateralvestibulardysfunction,suchasspontaneousbarrelrollingtowardstheexposuresidewhilewalking,wereseeninallanimalsexposedto3-NP(H)and40%(2/5)ofanimalsexposedto3-NP(L),exceptfortheoneanimaltreatedbilaterally,whichshowednosignsofimbalance.Bothnystagmusandposturaldisturbancesresolvedin2daysfollowing3-NPexposure.HistologicalstudyshowedtemporaryedematintheorganorCorti,Claudiuscellsandtheinnersulcuscells3daysafter3-NP(H)treatment.Enlargementofintercellularspaceinthespiralprominencewasfirstnoticedat12hourspost-3-NP(H)exposure,progressedatd
