简介：Objective:ToinvestigatetheeffectofRadixPaeoniaeRubra(RPR)ontheexpressionofhemeoxygenase(HO-1)andinducednitricoxidesynthase(iNOS)inendotoxin-inducedacutelunginjuryinratsanditsprotectivemechanism.Methods:FortyWistarratsweredividedrandomlyinto5groupswith8ratsineachgroup:salinecontrolgroup(NSgroup),lipopolysaccharidegroup(LPSgroup),RPR-treatmentgroup,RPR-preventiongroupandHemingroup.TheeffectofRPRonproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,malondialdehyde(MDA)contentinthelungandtheactivityofserumNOwereobserved.Arterialbloodwasdrawnforblood-gasanalysis.TheexpressionofHO-1andiNOSinlungtissueswasdetectedbyimmunohistochemitryandmorphometrycomputerimageanalysis.Thehistologicalchangesofthelungwereobservedunderlightmicroscope.Results:ComparedwiththatinNSgroup,theexpressionofHO-1andiNOSwasmarkedlyincreasedinLPSgroup(P<0.01).InRPR-treatment,RPR-prevention,andHemingroups,theexpressionofiNOSwassignificantlylower,whiletheexpressionofHO-1washigherthanthatinLPSgroup(P<0.05).Theproteincontent,theratioofneutrophilesinbronchoalveolarlavagefluid,thecontentofMDAandtheactivityofserumNOinLPSgroupweresignificantlyhigherthanthoseinNSgroup(P<0.01).TherewasasignificantdecreaseinthelevelofarterialbicarbonateandpartialpressureofoxygenintheLPSgroup(P<0.01);theseparametersoflunginjuryhowever,weresignificantlylowerinRPR-treatment.RPR-prevention,andHemingroupsthanLPSgroup(P<0.05orP<0.01).ThepathologicchangesoflungtissuesweresubstantiallyattenuatedinRPR-treatment,RPR-prevention,andHemingroupsthanLPSgroup.Conclusions:ThehighexpressionofHO-1reflectsanimportantprotectivefunctionofthebodyduringlipopolysaccharide-inducedacutelunginjury.TheprotectiveeffectofRPRonlipopolysaccharide-inducedacutelunginjuryisrelatedtotheinhibi

简介：Objective:Tostudythechangesofpartialpressureofbraintissueoxygen(PbtO2)andbraintemperatureinacutephaseofsevereheadinjuryduringmildhypothermiatherapyandtheclinicalsignificance.Methods:Onehundredandsixteenpatientswithsevereheadinjurywereselectedanddividedintoamildhypothermiagroup(n=58),andacontrolgroup(n=58)accordingtooddandevennumbersofhospitalization.WhilemildhypothermiatherapywasperformedPbtO2andbraintemperatureweremonitoredfor1-7days(mean=86hours),simultaneously,theintracranialpressure,rectumtemperature,cerebralperfusionpressure,PaO2andPaCO2werealsomonitored.Thepatientswerefollowedupfor6monthsandtheprognosiswasevaluatedwithGOS(Glasgowoutcomescale).Results:ThemeanvalueofPbtO2within24hourmonitoringinthe116patientswas13.7mmHg±4.94mmHg,lowerthanthenormalvalue(16mmHg±40mmHg)ThetimeofPbtO2recoveringtothenormalvalueinthemildhypothermiagroupwasshortenedby10±4.15hourscomparedwiththecontrolgroup(P<0.05).Thesurvivalrateofthemildhypothermiagroupwas60.43%,higherthanthatofthecontrolgroup(46.55%).Aftertherecoveryofthebraintemperature,PbtO2increasedwiththeriseofthebraintemperature.Conclusions:Mildhypothermiacanimprovethesurvivalrateofsevereheadinjury.ThetechniqueofmonitoringPbtO2andthebraintemperatureissafeandreliable,andhasimportantclinicalsignificanceinjudgingdiseaseconditionandinstructingclinicaltherapy.

简介：Objective:ToinvestigatetheeffectsofCO2pneumo-peritoneumonbloodflowvolumeofabdominalorgansofrabbitswithcontrolledhemorrhagicshockmodelandliverimpactinjuries.Methods:Aftercontrolledhemorrhagicshockandliverimpactinjuries,therabbitmodelwasestablished.Eighteenrabbitssubjectedtohemorrhagicshockandliverimpactinju-riesweredividedinto3groupsrandomlyaccordingtothevolumeoflostblood:lighthemorrhagicshock(bloodlossvolumewas10%,6ml/kg),moderatehemorrhagicshock(20%,12ml/kg)andseverehemorrhagicshock(40%,22ml/kg).IntraabdominalpressuresofCO2pneumoperitoneumwas10mmHg.Color-labeledmicrosphereswereusedtomea-surethebloodflowvolumeoftheliver,kidneyandstomachbeforepneumoperitoneumat30minutesand2hoursafterpneumoperitoneumand30minutesafterdeflation.Andthemortalityandhepatictraumaticconditionofrabbitswererecorded.Results:Ofthe18rabbits,therewere9withliverimpactinjuriesatGradeⅠ,8atGradeⅡandⅠatGradeⅢ(accordingtoAIS-2005).Themortalityrateinlighthemorrhagicshockgroupwas33.33%,andthatinmoderateorseverehemor-rhagicshockgroupwas100%within30minutesand2hoursafterpneumoperitoneum,respectively.Thebloodflowvol-umeintheorgansdetecteddecreasedat30minutesunderpneumoperitoneuminlightandmoderatehemorrhagicshockgroups.Atthesametime,thebloodflowvolumeoftheliverinmoderatehemorrhagicshockgroupdecreasedmoresig-nificantlythanthatinlighthemorrhagicshockgroup.Conclusions:ThebloodflowvolumeofabdominalorgansinrabbitsisdecreasedobviouslyunderCO2pneumoperitoneum,withfairlyhighmortalityrate.Itisbe-lievedthatCO2pneumoperitoneumshouldcautiouslybeusedinabdominalinjuryaccompaniedwithhemorrhagicshock,especiallyundernon-resuscitationconditions.

简介：Objective:Toinvestigatetheexpressionandpatternofvascularendothelialgrowthfactor(VEGF)anditsfetalliverkinase-1(Flk-1)receptorinspinalcordanddorsalrootgangliaafterneurotomyofsciaticnerveinrats.Methods:Forty-fiveadultmaleWistarratsweredividedrandomlyintoacontrolgroup(n=5)andanexperimentalgroup(n=40).ThebilateralsciaticnervesoftheratsintheexperimentalgroupunderwentneurotomyandtheL4-L6spinalcordandthecorrespondingdorsalrootgangliawereharvestedrespectivelyat8hours,and1,3,5,7,10,14and21days(8subgroupswith5ratseach)afteroperation.Theratsinthecontrolgrouponlyunderwentanexposureofsciaticnervewithoutneurotomy.ImmunohistochemistryandimageanalysiswereusedtostudytheexpressionofVEGFanditsFlk-1receptor.Results:BothVEGFandFlk-1receptorexpressedinthenormalratspinalcordanddorsalrootganglia.Inresponsetoneurotomy,theirexpressionreachedahigherlevelandpersistedforashorttimethendeclinedtothenormallevelrapidly.Besides,positivestainingofFlk-1wasobservedinbothglialcellsandnervefibers,whichlocatedinthewhitematterofthespinalcord.Conclusions:VEGFcanpromotetheregenerationofperipheralnervesfromtheangleofcentralneurons,whichestablishestheexperimentalandtheoreticalfoundationforVEGFtreatingperipheralnerveinjuries.