BACKGROUND:Recentstudieshaveindicatedthatblood-brainbarrier(BBB)disruptionfollowingsu-barachnoidhemorrhage(SAH)significantlycorrelateswiththedevelopmentofbraininjuryandpoorprognosisofpatientssubjectedtoSAH.OBJECTIVE:ToinvestigatebothfunctionalandstructuralchangesrelatedtoBBBinvariousphasesafterSAHinratsthroughquantitativeandqualitativemethods.DESIGN,TIMEANDSETTING:Thisexperiment,acompletelyrandomizeddesignandcontrolledex-periment,wasperformedattheDepartmentofNeurosurgery,theSecondAffiliatedHospitalofChongqingUniversityofMedicalSciencesfromJune2006toMarch2007.MATERIALS:Atotalof128female,healthy,Sprague-Dawleyratswereselectedforthisstudy.Mainreagentsandinstruments:EvansBluedye(SigmaCompany,USA),fluorescencespectrophotometer(ShimadzuCompany,Japan),andtransmissionelectronmicroscope(OlympusCompany,Japan).METHODS:Theincluded128ratswererandomlypidedintotwogroups:sham-operatedgroup(n=16)andSAHgroup(n=112).RatsintheSAHgroupwerepidedintosevensubgroups:6,12,24,36,48,60,and72hoursafterSAH(16ratsforeachtimepoint).ExperimentalSAHwasinducedbybloodinjectionintothepre-chiasmaticcistern(300μL).Thesham-operatedgroupreceivedanequivalentvolumeofnormalsalinesolution(300μL)injectedintothesubarachnoidspace.MAINOUTCOMEMEASURES:Braintissuewatercontentwasdeterminedbythewet-drymethod.BBBpermeabilityinthecerebralcortexwasdeterminedbyEvansBluedyeandfluorescentspectrophotometer.TheultrastructuralchangesinBBBwereobservedwithtransmissionelectronmicroscope.RESULTS:Comparedwiththesham-operatedgroup,SAHinducedasignificantincreaseinbrainwatercontentbetween24and60hours(F=888.32,P<0.05).Brainwatercontentincreasedtoamaximumby36hoursafterSAH,normalizingby72hours.EvansBluecontentinthecerebralcortexofSAHgroupratsbegantoincreaseby24hoursafterSAH,pea
