简介:Objective:Toevaluatetheefficacyandsignificanceofposterolateralfusioninpreventingfailureofshort-segmentstabilizationforthetreatmentofthoracolumbarburstfractures.Methods:Sixtypatientswiththoracolumbarburstfractureswereincludedinthestudy.Thepatientswereclassifiedintotwogroups(n=30ineachgroup).InGroupA,patientsweretreatedinourhospitalwithshort-segmentinstrumentationviaposterolateralfusionwithiliacbone.InGroupB,patientsweretreatedinotherhospitalwithshort-segmentfixationwithoutfusion.Allcasescametoourhospitalforreexamination.Therewere18malesand12femalesinGroupAwithameanageof42.3years(range,24to52years)and16malesand14femalesinGroupBwithameanageof41.5years(range,19to54years).Radiographic(Cobbangle,kyphosisofthevertebralbody,andsagittalindex)andclinicaloutcomes(LowBackOutcomeScore)wereanalyzedafteranaveragefollow-upof16months.Results:Afteroperation,Cobbanglewasreducedfrom19.3°to3.1°inGroupAandfrom19.1°to3.3°inGroupB(P>0.05).Itwas5.9°inGroupAand11.9°inGroupBatthefinalfollow-up(P<0.01).Itsaveragelossofcorrectionwas2.8°inGroupAand8.6°inGroupB.Averagekyphosisofthevertebralbodywasreducedfrom21.3°to6.2°inGroupAandfrom21.7°to7.4°inGroupB(P>0.05).Itwasdecreasedto7.9°inGroupAand13.5°inGroupBatthefinalfollow-up(P<0.01).Itsaveragelossofcorrectionwas1.7°inGroupAand6.1°inGroupB.Sagittalindexwasreducedfrom21.3°to3.6°inGroupAandfrom20.5°to3.8°inGroupB(P<0.05).Itwasdecreasedto5.1°inGroupAand9.8°inGroupBatthefinalfollow-up(P<0.01).Itsaveragelosswas1.5°inGroupAand6.0°inGroupB.InGroupA,73.3%ofpatientshadanexcellentresultbasedonLowBackOutcomeScoresystem,whilethatinGroupBwasonly43.3%.Conclusions:Posterolateralfusionisaneffectivemeasuretopreventimplantfailure,anddecreaselo
简介:Objective:toobserveeffectofendothelin-1(ET-1)onhepaticdamageinducedbyendotoxin.Methods:atotalof90ratswererandomlydividedintocontrolgroup(groupc),endotoxintreatedgroup(groupLPS)andendotoxinplusET-1antibodytreatedgroup(groupLEA).AnobservationwasdoneonthechangesofET-1concentration,andtranscriptionandexpressionofET-1mRNA.Plasmaglutamicpyruvictransaminaseenzyme(GPT),hepaticlactatedehydrogenase(LDH),adenosinetriphosphate(ATP)andmalondialdehyde(MDA)werealsoobservedat3,6,9,12,24hoursaftersaline,endotoxin(10mg·kg^-1)andET-1antibody(dalubine1:2000,2ml·kg^-1)administration.Results:TheresultsindicatedthattheconcentrationofplasmaandhepaticET-1andexpressionofET-1mRNAinliversignificantlyincreasedfollowingendotoxemia.ThehepaticET-1levelswereinverselycorrelatedwiththeATPconcentration,andpositivelyrelatedtotheMDAconcentration.ET-1antibodycouldpartiallyprotecttheliveragainstdamageinducedbyendotoxin.Conclusions:Theseresultssuggestthatendotoxinmay,ontranscriptionandtranslationlevel,leadtoanincreaseofET-1insynthesis.ET-1maycontributetohepaticdamageduringendotoxemia.
简介:Objective:Tostudytheeffectofmethylprednisolone(MP)onreperfusioninjuryinsevereuncontrolledhemorrhagicshockandexplorethepossiblemechanisminvolved.Methods:Twelvedogswererandomlydividedintotwogroups,controlgroup(GroupI,n=6)andMPgroup(GroupII,n=6).Theanimalswerebledcontinuouslyfromafemoralarterycathetertoproduceuncontrolledhemorrhagicshockmodels.ResuscitationwithlactatedRinger's(LR)solutionwasinitiatedwhenmeanarterialpressure(MAP)decreasedto20mmHg,andMAPwasmaintainedat30-40mmHg.MP(4mg/kg)wasinjectedintravenouslyinGroupIIwhenresuscitationbegan.WhileinGroupI,normalsaline(NS)wasinjectedinstead.Thelevelsofsuperoxidedismutase(SOD)andmalondialdehyde(MDA)weremeasuredbeforeexsanguination(T1),whenMAPdecreasedto20mmHg(T2),60min(T3)and120min(T4)afterresuscitation.Heartrate,MAPandcardiacoutput(CO)levelswererecordedconcomitantly.Results:InfusionvolumeandhemorrhagevolumeshedfromthesuperiormesentericarteryinGroupIwerehigherthanthoseinGroupII(P<0.01andP<0.05).Afterreperfusion,bloodSODlevelsdecreasedprogressivelyandMDAlevelsincreasedrapidlyinGroupI.InGroupII,bloodSODlevelsatT3andT4decreasedascomparedwiththatatT1butastepwiseincreasewaspresent.AtT4,bloodSODlevelwassignificantlyhigherinGroupIIthaninGroupI(P<0.01).AtT3andT4,MDAlevelsweremarkedlylowerinGroupIIthaninGroupI.Duringreperfusion,MAPwasmoresteadyinGroupIIthaninGroupIandsurvivalrateafter120min(atT4)washigherinGroupIIthaninGroupI(P<0.05).Conclusions:MPhasaprotectiveeffectonsevereuncontrolledhemorrhagicshockandsubsequentreperfusioninjury.Themechanismmainlyinvolvestheanti-lipidperoxidationactivityofMP.
简介:作者报导了支撑了臀部的无法缩减的postero侧面的创伤的脱臼与的一个27岁的人的案例胶囊并且labral陷阱。起始的X光显示出仅仅小acetabular碎片。在在一般麻醉下面与肌肉麻痹减少臀部的二次尝试失败了以后,病人被立即的开的减小通过一条postero侧面的途径对待。臀部的外科的探索表明小osteochondral碎片属于上唇和囊的一大片,堵塞髋臼。大腿骨的头与扭扣孔效果在撕的囊上交叉。这些元素被减轻,骨头碎片与2公里螺丝钉被修理,囊被修理。在10年的后续,功能的结果与100个点的一个哈里斯分数和坏死或骨关节炎的没有迹象是优秀的。作者建议这不平常的损害的文学评论。
简介:Objective:Toinvestigatetheproliferativeeffectofkeratinocytegrowthfactor(KGF-2)onhumanadultkeratinocytes.Methods:Thestandardmediumwaskeratinocytegrowthmediumwithoutbovinepituitaryextract(BPE),hydrocortisoneorepidermalgrowthfactor(EGF).Keratinocytesfroma48-year-oldsubjectwereculturedandseededondisheswithstandardmediumofEGFincelldensityof2×104/32mm2.After24hours,themediumwasreplacedbythestandardmediumwith0,4,16,125and500ng/mlKGF-2,respectively.ThestandardmediumwithEGFwasusedasthepositivecontrolandthestandardmediumwithoutEGForKGF-2wasusedasthenegativecontrols.Thegrowthofkeratinocyteswasmonitoredby3-(4,5-dimethythiazol-2-yl)-2,5dipheyltetrazoliumbromide(MTT)assayandbyphotographsondays3,5and7,respectively.Results:KGF-2inconcentrationsof4-500ng/mlshowedasignificantproliferativeeffectondays5and7ascomparedwiththatofthenegativecontrols(P<0.01).Onday3thecellswereproliferatedto1.5-2.5-fold,onday5to3-5-foldandonday7to3-12-foldinKGF-2mediumasthatofthenegativecontrols.TheoptimalresponseoccurredwhentheconcentrationofKGF-2was125ng/mlonday7.CellproliferationwasalsoconsistentlyhigherinallKGF-2concentrationsascomparedwiththatofthepositivecontrols.Conclusions:KGF-2hassignificanteffectsontheproliferationofadultkeratinocytes,whicharemoreeffectivethanthatofEGF.ThisstudysupportsKGF-2canimprovethehealingofchronicwoundsinadultsinclinic.
简介:Objective:Tostudytheclinicaltherapeuticeffectofanisodamineonrespiratoryfunctionafterseverebraininjury.Methods:Ninetypatientswithrespiratorydysfunctionfollowingseverebraininjuryweredividedintotwogroups:atreatmentgroup(n=45,treatedwithroutinetherapyplusanisodamine)andacontrolgroup(n=45,treatedwithroutinetherapyonly).Thepulmonaryventilationfunctionandoxygenationfunctionwerecomparedbetweenthetwogroups.Results:Inthetreatmentgroup,12hoursaftertreatmenttherespiratoryratereduced,thepartialpressureofcarbondioxide(PCO2),thepartialpressureofoxygeninarterialblood(PaO2)andoxygenationexponentincreased,thedeadspaceventilationdoseandthepulmonaryalveolus-partialpressureofarterialoxygendifferencedecreased,andtheventilationfunctionoftherespiratorytractandpulmonaryoxygenationfunctionimproved.Therewasasignificantdifferencebetweenthetwogroups(P<0.01).Noside-effectwasfoundexceptaslightincreaseofintracranialpressureandheartrate.Conclusions:Anisodaminecanimprovepulmonaryventilationfunctionandoxygenationfunctionanddecreasetheincidenceofhypoxemiamarkedly.Itiseffectiveintreatingrespiratorydysfunctionafterseverebraininjury.
简介:Objective:Tostudythechangeofthestressshieldingrateofstress-relaxationplateinvivoanditsinfluenceonfracturehealing.Methods:Thediaphysesofbilateraltibiasin70NewZealandrabbitswereosteotomizedandfixedwithstressrelaxationplates(SRP,theSRPgroup)andrigidplates(RP,theRPgroup),respectively.Thefracturehealingprocessinthese2groupswasinvestigatedbyradiography,lightandpolarizedlightmicroscopyandbiomechanicaltestat2to48weekspostoperatively.Results:Earlyafterfixationthestressshieldingratewasabout70%inbothgroups.WhileintheSRPgroupthestressshieldingratedecreasedgraduallyastimepassed,whyichwassignificantlylowerthanthatoftheRPgroup(P<0.05)bytheendofthe8thpostoperativeweek,andstabilizedatthelevelofabout27%at36-48weeksafterfixation.AbundantexternalcallusassociatedwiththeformationofcartilaginouscalluscouldbeobservedintheSRPgroupat2-4weekspostoperatively.Thetransformationofthecallusintothelamellarbonebeganat8-12weeks,thecollagengraduallyarrangedinorder,andthemechanicalnatureoftheunitedbonewasgraduallystrengthened,too.IntheRPgroup,theexternalcalluswasscarceattheearlystageoffracturehealing,andthecallusremodelingatthelatestageoffracturehealingwasdominatedbyboneabsorption.Theultimatebendingstrength(UBS)wasonly57.95%ofthatofthenormalby48weeks.Conclusions:ThedecreaseofthestressshieldingrateofSRPinvivowaswellinterrelatedwiththetimeoffixation.TheapplicationofSRPcouldpromotethecallusformationandbonereconstructionthustofavortherecoveryofthemechanicalstrengthoftheunitedbone.
简介:客观:为了调查汽车的效果,控制在试验性的骨折愈合和它的机制上锁钉子(AMLN)的微运动。方法:经历大腿骨的柄的横向的截骨术的双方的16只山羊分别地是有AMLN和Gross-Kempf(GK)钉子的固定intramedullary。后续时间是7,14,28和56天。Roentgenographic,简历机械,组织学,显微镜的扫描电镀物品和生物化学的分析是done.Results:(1)在在修理AMLN的组的fractural结束的反压缩,反屈曲和反扭转的力量比GK修理钉子的组的高;而,在折断的结束的压力躲蔽处的率显著地减少了(P<0.01)。(2)在修理AMLN的组的全部的骨胶原,不可溶解的骨胶原,钙和磷酸盐的内容在GK修理钉子的组比那高(P<0.05)。(3)胼胝的组织学的观察和定量分析表明AMLN能支持桥胼胝和骨膜胼胝的生长。因此愈合的制造和早完成的remolding过程,它比传统的GK好一些钉固定。(P<0.05)。(4)7-14天张贴操作,AMLN-fixedgroup的胼胝繁荣并且camellarly安排了,骨胶原纤丝在骨头trabecula的吸收空隙常常形成了。28-56天柱子操作,骨胶原纤丝是在吸收空隙附近繁荣并且与骨头平行“s纵的轴。活跃多骨的吸收和形成被看见,那么是remolding并且重建。Haversian系统是未经触动的,因为钙盐的免职,多骨的结构的网是很强的。任何一个都没在GK修理钉子的组上述调查结果被观察。结论:AMLN的设计与塑料固定理论一致很好。因为无变态的系统由theintramedullary固定仪器和破裂的近似、远侧的结束组成了的几何学是很坚挺的ands,搁置,到在fractural结束散布的物理压力的骚乱是轻的。在fractural部分之间的断断续续的物理压力的Thegeneration和行为能到达在压力行为和压力保护之间的平衡。特征愈合和remolding同时发生加快愈合的fractural过程。
简介:Objective:Toinvestigatethetherapeuticeffectofcisaprideongastricinjuryfollowinghemorrhagicshockresuscitation.Methods:108Wistarratsweighing(200g±30g)wererandomlydividedintoashamshock(SS)group(n=36),ahemorrhagicshockresuscitation(HS)group(n=36)andahemorrhagicshockcisapridetreated(HSC)group(n=36).Samplingat1,2and4hoursafterresuscitationwasdoneand6samplesforeachobservationitemweretaken.Thegastricbloodflowvolumewasmeasuredbyisotopelabelbiologicalmicroglobulin.GastricpHi,gastricemptying,MDAandNa+-K+-ATPaseofgastricmucosaweremeasured.Results:IntheHSCgroup,therelativeresidualrateofgastricpigmentdecreasedsignificantly,thegastricbloodflowvolumeelevated;gastricpHiincreasedsignificantlyat2hours;thelevelofmucosalMDAdecreasedat4hours,theactivityofNa+-K+-ATPaseincreasedandthelacticacidlevelintheportalveindecreasedsignificantlycomparedtotheHSgroup.Conclusions:Afterhemorrhagicshockresuscitation,cisapridecontainedthefollowingfunctions,1)promotinggastricemptying,2)increasingthebloodflowofgastricbloodflowvolumeandgastricpHi,3)depressingthelacticacidconcentrationoftheportalveinandimprovingMDAvolumeandNa+-K+-ATPaseactivityofgastricmucosa.Itsuggeststhataftercomplementingeffectivecirculatingbloodvolumeforhemorrhagicshockresuscitation,earlyuseofcisaprideforgastricmotilityishelpfulforanimprovementoflastingischemiaandhypoxiainstomach.
简介:Objective: Toreportamethodandremotetherapeuticeffectofearlynervetranspositionintreatmentofobstetricalbrachialplexuspalsy. Methods: FromMay1995toAugust1996,12patientswhohadnorecoveryofbiceps3monthsafterbirthweretreatedwithnervetransposition.Eighthadneuromaattheuppertrunkand4hadruptureoravulsionoftheuppertrunk.Mallettestwasusedtoevaluatetheresults. Results: Thefollow-upof40-52monthsshowedthatexcellentandgoodrecoveryinfunctionswasfoundin75%ofthepatientsandtheexcellentrateofphrenicnerveandaccessorynervetranspositionwas83.3%and66.7%respectively.Acompleterecoveryinshoulderandelbowjointfunctionwasin3patientsandMalletⅣwasin6patients. Conclusions: Satisfactoryoutcomecanbeobtainedbyusingearlynervetranspositionintreatingobstetricalbrachialplexus.Paralysis,obstetric;Peripheralnerves;Nervetransposition
简介:目的将在骨折和创伤的大脑损害(TBI)的设置以内观察浆液和胼胝leptin表示。64只男SD老鼠全部的方法A同等地被使随机化进4个组:nonoperated组,TBI组,破裂组,和fracture+TBI组织。老鼠在fracture+TBI以后在2,4,8和12个星期被牺牲。浆液leptin用放射性免疫测定被检测,并且胼胝形成放射学地被测量。胼胝leptin被immunohistochemistry分析。在破裂组,TBI组和联合fracture+TBI组的结果浆液leptin层次都显著地在2星期时间点与控制组相比被增加(P<0。05)。在联合fracture+TBI组的浆液leptin在在损害以后的4和8个星期在破裂和TBI组比那显著地高(P<0。05)。在fracture+TBI胼胝和胼胝体积的leptin积极的房间的百分比比在破裂唯一的组的那些显著地高(P<0。01)。我们在一只老鼠特别在开始的8个星期内在愈合的骨头以内表明了提高的leptin表示的结论骨折和TBI当模特儿。一个靠近的协会在破裂在leptin层次和胼胝形成的度之间存在。
简介:Objective:Tostudytheeffectofdecoy-oligodeoxynucleotides(decoy-ODNs)indumbbellshapewiththeoligodeoxynucleotidesequencesimilartonuclearfactorkappaB(NF-κB)cis-elementsonexpressionofinflammationmediatorsinpMΦcellsfromrats.Methods:Withcarriersofcationicliposomes,decoy-ODNsweretransfectedintopMΦcellsofrats.Thentheinhibitingeffectsofthedecoy-ODNsontumornecrosisfactorα(TNFα),interleukin-6(IL-6)andIL-10wereanalyzed.Results:Decoy-ODNscoulddecreasetheexpressionofTNFαandIL-6indose-dependentfashionbuthadweakerinhibitingeffectonIL-10.Conclusions:Decoy-ODNstargetingNF-κBcandecreasetheexpressionofinflammatorymediatorsinpMΦcellsfromrats.
简介:Objective:Todeterminetheefficacyofpolylacticacidglueinpreventingepiduralscaradhesionafterlaminectomyinrabbits.Methods:Twenty-fourJapanesewhiterabbitsunderwentlaminectomy(includingtheattachedligaments)atL2andL5.AfterlaminectomyatL5,polylacticacidgluewassprayedontheduraandnerverootsandthissegmentwastakenastheexperimentalgroup.AfterlaminectomyatL2,nothingwasusedandthissegmentwasenrolledastheselfcontrolgroup.Fourrabbitswerekilledeverytwoweekspostoperativelytilltheendoftheexperimentat12weeks.Thentheoperatedspinewasobservedgrossly,histologicallyandultrastructurallytocheckthedegreeofscarformation,thestatusofepiduralscaradhesion,theabsorptionoftheglue,andtheintracellularstructureoffibroblasts.Results:Thegluecoagulatedimmediatelyaftersprayingandshowedexcellenthemostaticeffect.Thegluemembranewaseasytobetakenawayfromtheduramaterofthesamplesfor2weeksandtherewerenocellsintheepiduralspaceintheexperimentalgroup.Buttheduramaterwascoveredbyhematomainthecontrolgroup,whichformedmildadhesion,withfibroblastsproliferatingactively.Inthe4thweek,someglueshiversremainedintheepiduralspacewithfibroblastsincreasingalittle,andtheduramaterwassmoothintheexperimentalgroup.However,inthecontrolgroup,theformedscarwasfragileandconglutinatedwiththeduramaterdiffuselyandfibroblastsweremuchmorethanthoseintheexperimentalgroup.Inthe6th-12thweeks,therewasapotentialinterspacebetweenthescarandtheduramater,andthepolylacticacidgluewasabsorbedcompletelyintheexperimentalgroup.Muchtoughscarwasfoundinthecontrolgroup,whichwasverydifficulttodissectfromtheduramaterandthesurroundingtissues.Fromtheultrastructuralobservationofthefibroblasts,thenucleusbecamemuchbiggerandtheroughendoplasmicreticulumwasmuchmoreplentifulinthecontrolgroupthanthatinthee
简介:Toexplorethemolecularmechanismoftheprotectiveeffectofnervegrowthfactor(NGF)oninjuredspinalcord.Methods:TheposteriorT8(the8ththoracicsegment)spinalcordsof60Wistarratswereinjuredbyimpactscausedbyobjects(weighing10g)fallingfromaheightof2.5cmwithAllensway.Solutionwithnervegrowthfactors(NGF)wasgivento30rats(theNGFgroup)throughamicrotubuleinsertedintothesubarachnoidcavityimmediately,andat2,4,8,12and24hoursafterspinalcordinjury(SCI)respectively.Normalsaline(NS)withsamevolumewasgiventotheother30rats(theNSgroup)withthesamemethod.And5normalratsweretakenasthenormalcontrols.Theexpressionofbcl-2andbaxproteinsinspinalcordwasdetectedwithimmunohistochemistry.Theapoptoticneuronsinspinalcordweremeasuredwithterminaldeoxynucleotidyltransferase-mediateddUTP-biotinnickend-labelingofDNAfragments(TUNEL)staining.Results:Thepositiveexpressionofbcl-2proteinwasstronginthenormalcontrols,butdecreasedintheNSgroup,andincreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Thepositiveexpressionofbaxproteinwasalsostronginthenormalcontrols,butincreasedintheNSgroup,anddecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).ApoptoticneuronswerefoundintheNSgroup,andtheydecreasedsignificantlyintheNGFgroupascomparedwiththatoftheNSgroup(P<0.01).Conclusions:NGFcanprotecttheinjurednervetissuesthroughstimulatingtheexpressionofbcl-2protein,inhibitingtheexpressionofbaxproteinandinhibitingtheneuronalapoptosisafterSCI.
简介:Objective: Toexplorethevariantprocessesofcellapoptosisandtheinhibitingeffectofmoderatehypothermiaoncellapoptosisafterdiffusebraininjury. Methods: ModelsofdiffusebraininjurywereinducedbythetraumadevicereportedbyMarmarou.1Atotalof128Wistarratsweredividedinto4groups:theuninjuredgroup(GroupA,n=8),theseverelyinjuredgroup(GroupB,n=60),themildlyinjuredgroup(GroupC,n=30)andthemildhypothermiagroup(GroupD,n=30).InGroupD,theseverelyinjuredratsweretreatedwithmoderatehypothermiatokeeptherectaltemperatureat32℃(standarddeviationfor0.1℃)for6hours.Thenthemorphosis,thecharacteristicsandthequantityofapoptoticcellsinthecerebralcortexandinthehippocampusregionsafterdifferentseveritiesofcraniocerebralinjurieswereobservedandcomparedunderanelectronicmicroscope,withterminaldeoxynucleotidylnickendlabeling(TUNEL)inDNAfragmentationandwithagarosegelelectrophoresis. Results: TUNELshowedapoptoticcellsincreasedaccordingtotheinjuryseverity,andtheypeakedat48hoursafterinjuryandthendeclined.InGroupC,apoptosiswaslocatedintheCA2andCA3areasofthehippocampus.AndinGroupB,apoptosisincreasedevidently,andlocatedinthewholehippocampusandinthefrontalandparietalcortexregions.Thehypothermia-treatedratshadsomeapoptoticcells,too.However,evenat24,48and72hoursafterinjurythereweresignificantlyfewerapoptoticcellsinthecortexandinthehippocampusinGroupDthanthatinthenon-treatedgroups.Electronmicroscopyshowedthattheapoptoticcellswereroundandshrunkeninmorphologyandthenucleiwereroundandcondensedat24and48hoursafterinjury.Andtheapoptosisat48hourswasmoreseverethanthatat24hours.Thehypothermia-treatedratshadnoapoptoticcells.GelelectrophoresisshowedthatcharacteristicDNA“ladders”wereobservedinthecortexandinthehippocampusat48hoursafters
简介:Objective:Toinvestigatetheinfluenceofintracranialpressure(ICP)andcerebralperfusionpressure(CPP)onneurologicaldeteriorationandoutcomeofseveretraumaticbraininjury(STBI).Methods:Atotalof245patientswithseveretraumaticbraininjurywerestudiedretrospectivelywithunivariateandmultivariatestudiestoevaluatethecontributionofICP/CPPtoneurologicaldeteriorationandoutcome.Results:Themortalityratesrosefrom16.2%in142patientswhosecourseofdiseasewassmoothto66.7%in103patientswhosufferedfromneurologicaldeterioration.Correspondingly,thefavorableoutcomefallfrom54.2%inthepatientswithoutneurologicaldeteriorationto18.3%inthosewithneurologicaldeterioration.Inthepatientswithclinicalevidenceofneurologicaldeterioration,therelativeinfluenceoftheICPandtheCPPonoutcomewasassessed.Themosepowerfulpredictorsofneurologicaldeteriorationwasthepresenceofintracranialhypertension(ICP>30mmHg,1mmHg=0.133kPa).TheCPPalsohadaprognosticpoweronneurologicaldeteriorationwhenitslevellessthan60mmHg.Conclusions:Itsuggeststhatit'sveryimportanttolowertheintracranialhypertensionandkeeptheCPPnotlessthan60mmHgduringthetreatmentofSTBI.
简介:Objective:Toinvestigatetheeffectofmoderatehypothermiaonresponsesofaxonalcytoskeletontoaxonalinjuryintheacutestageofinjury.Methods:Offifteenadultguineapigs,twelveanimalsweresubjectedtostretchinjurytotherightopticnervesanddividedintothenormothermicgroup(n=6)inwhichtheanimal'scoretemperaturewasmaintainedat36.0-37.5℃andthehypothermiagroup(n=6)inwhichthecoretemperaturewasreducedto32.0-32.5℃afterstretchinjury.Remainingthreeanimalssustainednoinjurytotherightopticnervesandservedascontrolgroup.Halfofinjuredanimals(n=3)ofeithernormothermicgrouporhypothermicgroupwerekilledateither2hoursor4hoursafterinjury.Theultrastructuralchangesofaxonalcytoskeletonoftherightopticnervefibersfromtheanimalswereexaminedunderatransmissionelectronmicroscopeandanalyzedbyquantitativeanalysiswithacomputerimageanalysissystem.Results:At2hoursafterstretchinjury,therewasasignificantreductioninthemeannumberofmicrotubules(P<0.001),andasignificantincreaseinthemeanintermicrotubulespacing(P<0.05orP<0.01)inaxonsofallsizesinnormothermicanimals.Themeannumberofneurofilamentsalsodecreasedstatistically(P<0.01)inlargeandmediumsubgroupsofaxonsinthesameexperimentalgroupat2hours.By4hours,thelargesubgroupofaxonsinnormothermicanimalsstilldemonstratedasignificantdeclineinthemeannumberofmicrotubules(P<0.01)andanincreaseinthemeanintermicrotubulespacing(P<0.05),whilethemediumandsmallsubgroupsofaxonsdisplayedasignificantincreaseinthemeannumberofneurofilaments(P<0.05)andreductioninthemeaninterneurofilamentspacing(P<0.05).Onthecontrary,eitherthemeannumberofmicrotubulesandthemeanintermicrotubulespacing,orthemeannumberofneurofilamentsandinterneurofilamentspacinginaxonsofallsizesinhypothermicstretch-injuredanimalswasnotsignificantdifferentfromthemeanvaluesofsham-operated