1/1持續(xù)性壓迫對損傷脊髓組織學變化的影響持續(xù)性壓迫對損傷脊髓組織學變化的影響TheeffectsofpersistentoppressiononthelesionofthespinalcordUpdatedate:2010-07-03withdaweiwumeimei【abstract】objectivetoobservetheeffectofcompressiononthebloodflowandpathologicalchangesofspinalcordafteracutespinalinjury.Methodsthebloodflowdeterminationofthespinalcordinthespinalcordoftheacutespinalinjuryandtheanimalandnon-oppressedgroupweremeasured,andthephotoscopeandelectronmicroscopywereobserved.Results(1)thereductionofbloodflowrateofthespinalcordinacuteinjurywasnotsignificant,butitaffectedtherecoveryofbloodflowintheinjuredspinalcord.(2)prolongedcompressionofthespinalcordpathologicalchangesoftheinjuredpartofthespinalcord.Conclusionsustainedcompressionofspinalcordinjuryistheresultofslowrecoveryofbloodflowinthespinalcord.【keywords】acutespinalcordinjuryoppressingthespinalcordbloodflowtissuepathologicalchangesEffectofContinuedCompressiononHistopathologicChangesAfterSpinalCordInjuryCHUtong-wei,WUMei-ying,MAshu-zhi,etalDept.OfOrthopaedics,XinqiaoHospital,ThirdMilitaryMedicalUniversity,Chongqing400037【Abstract】AimTostudytheeffectofcompressiononthelocalbloodflow,andthehistopathologicchangesoftheinjuredspinalcord.MethodsThebloodflowwasmeasured,andthehistopathologicchangesunderlightmicroscopeandelectronmicroscopeoftheinjuredspinalcordinbothofthecompressedgroupandthenon-compressedgroupwereobserved.Results(1)Thecompressiondidnotaffectthedecreasingrangeoftheinjuredspinalcordbloodflow.(2)Long-termcompressioncausedcontinuousdamagetotheinjuredspinalcord.ConclusionContinuedcompressionaggravatespathologicinjurythroughaffectingtherecoveryoflocalspinalcordbloodflow.SpinalcordBloodflowHistopathologicchangePathologicalchangesafteracutespinalcordinjury(sci)hasbeenwidelystudied,butexistsafteracutespinalcordinjuryofoppressiontotheimpactofspinalcordtissuepathologicalchangeshasnotyetbeenreported.Becauseofthesuddenonsetofthespinalcordinjurycausedbytheclinicalpatient,thefractureblockisoftenremovedintothespinalcanalandthespinalcordbecomessecondary.Inordertoexploretheinfluenceofoppressiononthespinalcordinjury,thispaperhascarriedoutapreliminarystudytoprovideexperimentalbasisforthetreatmentofpatientswithclinicalspinalcordinjury.MaterialsandmethodsThepreparationofanimalgroupsandmodelsGroupofanimals:healthyJapanesebigearswhiterabbit62,maleandfemale,weight2.5~3kg.Randomlydividedintothespinalcordandthecompressiongroup(hereinafterreferredtoasthecompressiongroup),thenumberofrabbits=28;Thepurespinalsideimpactgroup(hereinafterreferredtoasthenon-oppressivegroup),thenumberofrabbits=28;Thecontrolgroup,thenumberofrabbitsis6.Preparationofthemodel:theanimalwasgivena2.5mg/kgofsodiumpentobarbital.Thebackhairisdepilate,thesterileconditionisexposedthewaist45rightvertebraplate,inthewaist5vertebraarchrootopenwindow,putthedamagehook.Thenon-oppressivegrouponlyusedthe[1]spinalsideimpactor,whichwasusedbythestateauxiliary,tocausetheanimaltobeparaplegic;Thecompressiongroupadoptedthestateauxiliaryexperimentalmethodtocausethereversibleparaplegic,andthenplacedtheself-madecementcompressionintheareaofthespinalcordinjury.Thecompressionissemi-cylindrical,0.5cmlong,0.2cmwideand0.15cmhigh.Figure1showstheCTscanoftherabbit’sspinalcanalwiththecompressionofthespinalcord.Thecontrolgroupsimulatedtheprocedureofthepreparationofanimalmodelsandthenmeasuredtheamountofgraybloodflowinthespinalcordasanormalcontrol.Aftertheoperation,theskinwassuturedandthemuscleswereinjectedwithpenicillin(400,000units/day)topreventinfectionafteroperation.Figure1putspressureontherabbit’sspinalcanalBloodflowmeasurementandpathologicalobservationofspinalcordModelpreparation,6,24,72in2hours,respectively,after1week,3,64fromeachrabbithydrogenclearancemethod(PHG-300bloodflowmeter,Japan)todeterminetheflowofbloodtotheinjuryofspinalcordgreymatterandthentaketheinjuryofspinalcordlineelectronmicroscopyandlightmicroscopyobservation,respectively.Third,statisticsprocessingThet-2program,whichwasdevelopedbythethirdmilitarymedicaluniversity,wascarriedoutfort-testandsinglefactorvarianceanalysis.TheresultsofAchangeinbloodflowThevariationofbloodflowintheexperimentalgrouprabbitspinalcordwasseenintheattachedtable.Tablerabbitspinalbloodflowchanges(ml.Min-1.100g-1)GrouptimeafterinjuryTwohours,sixhours,sixhours,twohours,twohours,threeweeks,threeweeks,sixweeksControlgroup72.38plusorminus1.9972.38+/-1.9972.38+/-1.9972.38+/-1.9972.38+/-1.9972.38+/-1.9972.38+/-1.99Thecompressiongroupwas43.38++1.6437.90+/-1.3154.67+/-1.89delta58.46+/-1.81delta62.78+/-1.55delta66.56+/-1.14delta70.52+/-1.60deltaNon-oppressivegroup45.19++1.5636.96+/-1.2547.37+/-1.65delta49.87+/-1.33delta54.47+/-1.63delta56.16+/-0.99delta57.10+/-1.62deltaAtthesametime,thephasepointcomparesdeltaP0.05Organizationalpathologicalchanges1.Thenchange:oppressionandrepressiongroup1weeksthenpathologicalchangesnotobviouslydifferent,performancefor2hoursafterinjurysubarachnoidandgraymatterhemorrhage,edema;6hoursafterinjuryofneuronsinnecrosis,themajorityofneuronsinischemicchange,characterizedbycellshrinkage,interstitialedema,whitematteredemaofmyelin.Thisphenomenonisstillevidentinoneweek.Thepathologicalchangesofthespinalcordwereimprovedafter1week,andtheappearancewasnormalin6weeks.After1weekofcompression,thespinalcordwasdamagedbytheprogressivestructure,andin6weeks,alargenumberofneuronswerelostandthemyelinstructurewasdamagedinahoneycomb(figure2).FIG.2.Thespinalcordofthespinalcordwaswidelylostduringthe6thweekofthecompressiongroup.Whitematteredemawasahoneycomb,HE*2002.Thechangesunderelectronmicroscope:injuryofspinalcordcompressiongroup,deformationcapillariesintheflat,lumenvisibleinplateletaggregation,ratherthantheoppressedgroupdidnotseethisphenomenon,thismaybeassociatedwithoppression(figure3).Intheperiodof2hoursto1weekaftertheinjury,thepathologicchangesofthespinalcordwerecharacterizedbythedegenerationofneuronaldegenerationandthetranssexualnecrosisofnervefibers.First,thechangessuchastheexpansionoftheinnermassnet,thechromatinsidesetandthenuclearfragmentationareseenintheneuron.Themyelinsheathisalittletoolateforischemia.Withinsixhours,themitochondrialcrestintheneuronisvisibleandcavitated,andthemyelinsheathfractures.Thespinalcordedemaandstructuraldamageofthegroupandnon-oppressedgroupwerereducedin1week.Thestructureofthespinalcordinthespinalcordwassignificantlydecreasedinthespinalcordofthespinalcordoftheinjureddivisionofthegroupin3weeks,andthestructureoftheresidualneuroninthespinalcordwasnormalin6weeks.Thedamagetothespinalcordinthecompressiongroupcontinueduntil6weeksaftertheinjury,andalipidcavitationwasfoundintheresidualneuronsintheinjuredpart(FIG.4).FIG.3.Thecapillariesofthespinalcordweredeformedby2,950Thelowdensitylipidcavitationintheneuronwithin6weeksofthecompressiongroupdiscussInpatientswithacutespinalcordinjury,thespinalfractureisoftenfollowedbyspinalfractureanddislocationofthespinalcord.Forpatientswithincompleteparaplegia,surgicaldecompressiontherapyisstilloneofthemainapproachestoclinicaltreatment.However,thereisnoexperimentalstudyoftheimpactofcompressiononspinalcordinjury.Theexperimentalresultsconfirmedthatoppressionandrepressiongroup6hoursafterspinalcordinjurylocalbloodflowdecreasedtothelowestpoint,twogroupsofmeantherewasnosignificantdifference(P0.05).Inthefuture,Thebloodflowofthespinalcordinthenon-oppressedgroupwasrestored,andthenormallevelwasreachedat6weeks.Oppressiongroupinjuryofspinalcordbloodflowandthepressurerisetrendatthesametime,butfarlessthanthespeedofcompressionset,recoveryandcompressionsetisin1weekaftereachphasepointshowedatrendofstagnationofbloodflowtoincreasespeed.Thisreflectsthedecreaseinbloodflowrateoftheinjuredspinalcord,butpreventstherecoveryofbloodflowintheinjuredpartofthespinalcord.Thecauseofthereductioninthereductionofbloodflowintheinjuredpartofthespinalcordmaynotbeassevereastheacuteimpairmentcausedbythecompressionofthespinalcord.Thevasculardeformationofthespinalcordoftheoppressedgroupmayberesponsiblefortheslowingandstagnationoftherecoveryofbloodflowinthespinalcord.Withinafewhoursafteracutespinalcordinjury,spinalcordthemainpathologicalchangesofthecentraltube,nearandthegraymatterhemorrhage,edema,thentheinjuryofspinalcordinvolvement[2,3].Thispathologicalprocesswascompletelyrepeatedbythespinalcordofthecompressiongroupandthenon-oppressedgroup.Oppressionandrepressiongroupinjuryofspinalcordpathologicalchangeswereobservedunderlightwithin1weeksdidnotsee,showedtheoppressiontotheimpactofspinalcordinjurydepartmentfailedtowithin1weekthenshowedobviouspathologicalchanges.After1week,thespinalcordofthenon-oppressedgroupwasimproving,andthephotoscopeofthespinalcordandelectronmicroscopywerenormalat6weeks.Buttheinjuryofspinalcordcompressiongroupisprogressivestructuralfailure,6weeksthenseeinjuryofspinalcordgreymatterwithinalargenumberofneuronsdepigmentation,whitematterinmyelindestroyahoneycombstructure;Thepresenceoflipidcavitationintheneuronsundertheelectricmirrorisassociatedwithalackofoxygeninthebloodsupplyofneu