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1、第26卷第4期西安交通大学学报(医学版)Vol.26No.42005年8月JournalofXi'anJiaotongUniversity(MedicalSciences)Aug.2005重症急性胰腺炎胰腺损伤与肺损伤的关系刘学民,潘承恩,刘青光,徐军,徐高峰,张梅(西安交通大学第一医院肝胆外科,陕西西安710061)摘要:目的探讨重症急性胰腺炎(SAP)引起急性肺损伤(ALI)的机制。方法48只实验组大鼠注射40g/L(4%)牛磺胆酸钠制作SAP模型。实验组及对照组(48只)大鼠分别在1、3、5、7、9、12h点剖杀,取
2、胰腺及肺组织行病理观察、微血管通透性及MPO活性测定;RT-PCR法检测胰腺及肺组织中细胞间黏附分子(ICAM-1)、肿瘤坏死因子(TNF-α)基因表达。结果制模后胰腺及肺损伤逐渐加重,胰腺及肺髓过氧化物酶(MPO)活性及微血管通透性逐渐升高;胰腺TNF-α、ICAM-1基因表达均在1h明显升高,至7h达到峰值;肺组织TNF-α、ICAM-1基因表达则在1h后逐渐上升,至9～12h达到峰值。结论SAP引起ALI过程中存在明显的时间窗口,该窗口内的早期预防性保护可能利于防止ALI的发生。关键词:机制;重症急性胰腺炎;急性肺损
3、伤;TNF-α;细胞间黏附分子中图分类号:R576文献标识码:A文章编号:1671-8259(2005)04-0371-03RelationshipbetweenpancreasandlunginjuryinsevereacutepancreatitisLiuXuemin,PanCheng'en,LiuQingguang,XuJun,XuGaofeng,ZhangMei(DepartmentofHepatobiliarySurgery,FirstHospitalofXi'anJiaotongUniversity,Xi'an
4、710061,China)ABSTRACT:ObjectiveTostudythepathogenesisofacutelunginXuryinsevereacutepancreatitis(SAP).MethodsToinduceSAPmodel,48ratsweretreatedwith4Ysodiumtaurocholate.SAPandcontrolratsweresacrificedat1,3,5,7,9and12hours.Pancreasandlungtissuewereobtainedforpatholog
5、icalstudy,microvascularpermeabilityandmyeloperocidase(MPO)examination.Geneexpressionoftumornecrosisfactor(TNF-α)andintercellularadhesionmolecule(UCAM-1)inpancreasandlungtissuewasdetectedbyRT-PCR.ResuItsAfterSAPmodelwasestablished,theinXureddegreeofthepancreasandth
6、elungincreasedgradually,accompaniedwithgradualincreaseofMPOactivityandmicrovascularpermeability.GeneexpressionofTNF-αandUCAM-1inpancreasincreasedat1hourandreachedpeakat7hours.Relatively,theirgeneexpressioninthelungonlyincreasedslightlyat1hourandreachpeakat9-12hour
7、sgradually.ConcIusionThereisanobvioustimewindowofinXurybetweenpancreasandlunginSAP,andearlierprotectionisbeneficialtopreventtheoccurrenceofacutelunginXury.KEYWORDS:pathogenesis;severeacutepancreatitis;acutelunginXury;tumornecrosisfactor;intercellularadhesionmolecu
8、le重症急性胰腺炎(severeacutepancreatitis,制研究对于其临床诊治有重要的意义。SAP)时急性肺损伤(acutelunginjury,ALI)是常见1材料与方法而严重的并发症,是肺炎症和肺微血管通透性增加的急性、进行性缺氧性呼吸衰竭,其最终阶段即为急性1.1实验动物及分组实验大鼠由
