BNP在膿毒癥中的研究進(jìn)展

BNP在膿毒癥中的研究進(jìn)展B(B-typenatriuretic的合成及分泌主要在心室，其目前是心衰診斷、[1]，而越來越多的研究顯示BNPBNP在膿毒癥中的研究進(jìn)展作一綜述。一、BNP的病理生理特性BNP1988Sogoh等[2]從腦組織中分離出來，其由32個(gè)氨基酸組成，多肽結(jié)構(gòu)和藥理學(xué)活性與心房利鈉肽極為相似，多由心室肌細(xì)胞合成和分泌，主要在翻譯水平進(jìn)行調(diào)控。刺激BNP基因表達(dá)及分泌增高的因素主要為物理（心室機(jī)械牽張）、化學(xué)（暴露于腎素系統(tǒng)BNP具有利鈉、利尿、擴(kuò)張血管、抑制腎素醛固酮系統(tǒng)、抑制促腎上腺皮質(zhì)激素的釋放及交感神經(jīng)的過度反應(yīng)等作用，參與調(diào)節(jié)血壓、血容量及鹽平衡。有研究顯示BNP二、BNP在膿毒癥時(shí)的變化及其可能機(jī)制血漿BNPBNP。因此，BNP[4]。BNP[5]。膿毒癥時(shí)釋放的炎IL-6、、TNFα等可直接抑制心肌收縮功能，并激活腎素血管緊張素以及交感神經(jīng)[6]。膿毒癥導(dǎo)致的雙心室擴(kuò)張是使BNPBNP[7]BNPLVEFLVEF好轉(zhuǎn)濃度降低。然而，近年來越來越多的研究發(fā)現(xiàn)，在無心功能收縮障礙的膿毒癥患者中BNPBNP的升高存在另外的機(jī)制。已有多個(gè)體外實(shí)驗(yàn)證實(shí)某些促炎癥因子如IL-1、IL-6，TNFαBNP增加[8-10]，提示炎癥反應(yīng)可能是BNP分泌的另一重要機(jī)制，膿毒癥時(shí)產(chǎn)生的內(nèi)毒素以及炎BNP的合成。Meader8BNP水500pg/ml[11]。Renana等[12]BNP升高但并不伴有心功能不全，BNPCRPBNP升高有一定作用，炎癥因子可促使心臟分泌BNP。McLean[14]進(jìn)一步證實(shí)在心功能正常的膿毒癥患者中，炎癥反應(yīng)可直接誘導(dǎo)BNP的升高。三、BNP在膿毒癥的診斷及判斷預(yù)后中的應(yīng)用BNP作為診斷和監(jiān)測(cè)膿毒癥時(shí)心功能的指標(biāo)BNP。嚴(yán)重膿毒癥時(shí)BNP4190pg/ml[16]BNPLVEF的減退,LVEF好轉(zhuǎn)其濃度減少。Jefic[17]PAWPPAWP患[18]PAWP在重癥患者當(dāng)中的應(yīng)用需謹(jǐn)慎。另外，進(jìn)來越來越多的研究發(fā)現(xiàn)膿毒癥患者血BNP升高但并不伴有心功能不全，炎癥反應(yīng)對(duì)BNP升高亦起作用，這也表明，與肌鈣蛋白不同，BNP作為診斷和監(jiān)測(cè)膿毒癥時(shí)心功能的指標(biāo)目前存在一定缺陷。膿毒癥的危險(xiǎn)分層及預(yù)后對(duì)于BNP有的18]BNPCuthbertson等[21]則發(fā)現(xiàn)膿毒癥患者存活組的BNP值明顯高于非存活組，得出了相反的結(jié)論。另外一些研究[22、17]認(rèn)為膿毒癥患者BNP值與其預(yù)后無任何相關(guān)性。BNPYucel[19]研APACHEII、、cTnICRP的升高均可用來預(yù)測(cè)膿毒癥患者的死亡[14]1000例就診于北京朝陽(yáng)醫(yī)院急診室的病人進(jìn)行研究，發(fā)現(xiàn)在SIRSBNP的陽(yáng)性檢測(cè)率高于非SIRSBNPAPACHEIIBNP>113pg/mL是膿毒癥患者死亡的獨(dú)立預(yù)測(cè)因子，鑒于其敏感性不高，研究者提議可將APACHEII評(píng)分和BNP2011年，Perman825SIRS診斷或可疑感染的病人，發(fā)現(xiàn)BNP[20]，提示BNP水平可以對(duì)膿毒癥患者進(jìn)行危險(xiǎn)分層。綜上所述，膿毒癥患者BNP水平升高不僅與心血管功能有關(guān)，也與系統(tǒng)性炎癥反應(yīng)相關(guān)。BNP的合成也可由內(nèi)毒素和炎癥介導(dǎo)。BNP可以作為識(shí)別膿毒癥誘導(dǎo)心功能不全的較可靠指標(biāo)，并可作為膿毒癥的一個(gè)預(yù)后標(biāo)志。參考文獻(xiàn)WieczorekSJ,WuAH,ChristensonR,etal.ArapidB-typenatriureticpeptideassayaccuratelydiagnosesleftventriculardysfunctionandheartfailure:amulticenterevaluation[J].AmHeartJ2002;144(5):834-9.SogohT,KangawaK,MinaminoN,etal.Anewnatriureticpeptideinporcinebrain.Nature,1988,332:78–81CostelloLC,BoerrigterG,BurnettJrJC.Revisitingsaltandwaterretention:newdiuretics,aquaretics,andnatriuretics.MedClinNorthAmDeLemosJA,McGuireDK,DraznerMH.B-typenatriureticpeptideincardiovasculardisease.Lancet2003;362(9380):316-22.McLeanAS,TangB,NalosM,etal.IncreasedB-typenatriureticpeptide(BNP)levelisastrongpredictorforcardiacdysfunctioninintensivecareunitpatients.AnaesthIntensiveCare,2003,31:21-27.Torre-AmoineG,KapadiaS,BenedctC,OralH,YoungJB,MannDL.Proinflammatorycytokinelevelsinpatientswithdepressedleftventriculardysfunction.JAmCollCardiolWitthautR,BuschC,FraunbergerP,etal.Plasmaatrialnatriureticpeptideandbrainnatriureticpeptideareincreasedinsepticshock:Impactofinterleukin-6andsepsisassociatedleftventriculardysfunction.IntensiveCareMed,2003,29:1696-1702.HeQ,LaPointeMC.Interleukin-1betaregulatesthehumanbrainnatriureticpeptidepromoterviaCa2+-dependentproteinkinasepathways.Hypertension,2000,35(12):292-296.KuwaharaK,SaitoY,HaradaM,etal.Involvementofcardiotrophin-1incardiacmyocyte-nonmyocyteinteractionsduringhypertrophyofratcardiacmyocytesinvitro.Circulation,1999,100:111-6.MaKK,OgawaT,deBoldAJ.Selectiveupregulationcardiacbrainnatriureticpeptideattranscriptionalandtranslationallevelsbyproinflammatorycytokinesandbyconditionedmediumderivedfrommixedlymphocytereactionsviap38MAPkinase.JMolCellCardiolApr2004;36(4):505–13.））MeaderM,AmmannP,KiowskyW,RickliH.B-tipenatriureticpeptideinpatientswithsepsisandpreservedleftventricularejection.EurJHeartFailRenanaShor,YosephRozenmanB,AharonBolshinsky.BNPinsepticpatientswithoutsystolicmyocardialdysfunction.EuropeanJournalofInternalMedicine,2006,17:536-540.McLeanAS,HuangSJ,HyamsS,etal.PrognosticvaluesofB-typenatriureticpeptideinseveresepsisandsepticshock.CritCareMed2007;35(4):1019-26.ChenL,LiC.SignificanceofBNPobtainedintheemergencydepartmentinpatientswithSIRSorsepsis.AmJEmergMed2009.WitthautR,BuschC,FraunbergerP,etal.Plasmaatrialnatriureticpeptideandbrainnatriureticpeptideareincreasedinsepticshock:Impactofinterleukin-6andsepsisassociatedleftventriculardys2function.IntensiveCareMed,2003,29:1696–1702CharpentierJ,LuytCE,FullaY,etal.Brainnatriureticpeptide:amarkerofmyocardialdysfunctionandprognosisduringseveresepsis.CritCareMed,2004,32(3):660-665.JeficD,LeeJW,Savoy-MooreRT,RosmanHS.UtilityofB-typenatriureticpeptideandN-terminalproB-typenatiureticpeptideinevaluationofrespiratoryfailureincriticallyillpatients.Chest2005;128(1):288–95.TungRH,GarciaC,MorssAM,PinoRM,FiferMA,ThompsonBT,etal.UtilityofB-typenatriureticpeptidefortheevaluationofintensivecareunitshock.CritCareMed[19]TYucel,DMemi?,BKaramanl?oglu,NSüt,MYuksel.Theprognosticvalueofatrialandbrainnatriureticpeptides,troponinIandC-reactiveproteininpatientswithsepsis.ExpClinCardiol2008;13(4):183-188.SarahM.Perman,MD,MS,AnnaMarieChang,MD,JuddE.Hollander,MD,etal.RelationshipBetweenB-typeNatriureticPeptideandAdver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