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论著2007年12月第4卷第34期慢性肝损伤家兔胆石症模型制作及成石因素研究俞渊’，唐乾利，，赫军（1.广西中医学院第一附属医院，广西南宁，黄名成’，王清坚，，关中正z530023；2.广西中医学院，广西南宁530001）【摘要】目的：建立四氯化碳（CCI。）所致慢性肝损伤、肝硬化大耳白兔模型，在此基础上研究CCl。所致慢性肝损伤的胆囊结石情况，探讨慢性肝损伤家兔胆囊结石形成的机制，从而论证采用慢性肝损伤家兔建立胆石症模型的可行性。方法：将50只家兔随机分成正常组、高胆同醇膳食组、慢性肝损伤组、肝硬化组、肝损伤后胆固醇组。观察家兔的胆石形成情况，透射电镜观察肝细胞超微结构，抽取胆汁细菌培养，酶比色法检测胆囊胆汁中胆汁酸、胆同醇的含量。结果：正常组无一例成石，高胆同醇膳食组8／8成石，慢性肝损伤组5／8成石，肝硬化组6／7成石，肝损伤胆固醇组6／8成石。慢性肝损伤组、肝硬化组、高胆同醇膳食组、肝损伤胆同醇组4组中肝脏超微结构均发生不同程度异常改变，以肝细胞水肿变性、核膜呈锯齿状、粗面内质网增多、线粒体肿胀为多见，肝硬化家兔组可见肝细胞凋亡坏死.高胆同醇膳食组可见胞质中大量脂滴。各组细菌培养均未发现细菌生长。慢性肝损伤组、肝硬化组胆囊胆汁中胆汁酸、胆同醇的含量均较正常组降低。结论：皮下注射CCl。致家兔肝损伤，进而诱导胆囊结石的造模方法可靠。形成的结石为混合性结石。慢性肝病所致肝细胞超微结构异常引起胆汁成分的改变，是肝病患者易发生胆石症的主要原因。慢性肝损伤、肝硬化与胆石症的发生有密切关系，且随着肝脏病变的加重，成石率升高。细菌感染可能不是慢性肝损伤胆囊结石的独立致石因素。[关键词卜陵性肝损伤；胆石症；肝细胞超微结构；动物模型【中图分类号】R575【文献标识码】A[文章编号】1673―7210（2007）12（a）一106一04TobuildthecholelithiasismodelinrabbitswithCCl4andresearchthepathogenenesis0fcholelithiasisYUYttoltl,TANGQian-li’，HEJun|，HUANGMing-weil，WANGQin!卜；ian+,GUANZhong-zhen毒（1.TheFirstAffiliatedHospitalofGuangxiTraditionalChineseMedicalUniversity，Nanning530023。China：2.GuangxiTraditionalChineseMedicalUniversity，Nanning530001，China）[Abstract]Objective：Todiscusstherelationthatchronicliverinjuryandcirrhosiscausedbvcarbontetrachloride（CCl4）.StudythechronicliverinjurycausedbyCCl4whethercouldleadtogallstone，whichprovethefeasibilitvthatbuildtherabbitmodelbymeansofchronicliverinjury.Methods：50rabbitsweredividedinto5groupsstochastic.Nonnalcontrolgroup，thehighcholesteroldietgroup，thechronicliverinjuresgroup，thecirrhosisoflivergroup，thegrouPthatcholesterincalculusafterchronicliverinjures.Wemadeuseofbiochemicalparametertoobservethechangingofbilecompositionandthefunctionalofliver.Weusedthelightmicroscopeandtheelectronicmicrosopetoobservethepathologicalchangeoftheliverhypodermicandtheuhrastructure.Toobservetherateofgallstoneformation，anddiscusstheinfluencethatthehighcholesteroldiettotherateofgallstoneformationafterliverinjury.Results：Therewasnotanygallstonefoundinthenor―malcontrolgroup.Stoneswereseeninthegallbladderof8／8inthehighcholesteroldietgroup，4／8inthechronicliverin―jurygroup，6／7inthelivercirrhosisgroup，6／8inthegroupthatcholesterolcalculusafterchronicliveriniury.TheanomalvchangesofliveruhrastructurehadoccurredinallthemodelgToup.Wecouldseethehepatocytehydropicdegeneration.thekaryothecachangetoserrationform，themitochondriontumefaction，theRERmanifold.Thehepatoeyteturnedtoapoptosl‘sinthelivercirrhosisgroup，thereweregreatdealoflipiddropletincytoplasminthehighcholesteroldietgrouD.Thegrowthofbacteriainthebacterialculturemedia.wasnotfoundThelevelofcholesterolandTBAingall。thechronicliverinjurygroupandlivercirrhosisgroupwerelowerthanthenormalcontrolgroup.Conclusion：It’scredibletobuildtherabbitmodelthatliverinjuryledtothecholelithiasisbymeansofhypoCCl4.Andtheprope~yofstoneisml’xedcomposi―tion.Thechangeofcomponentofthegallandthedecreaseofliverfunctionaretheprimaryreasonthatthecholelithiasisandthehepaticdiseaseareoftenconcurrence.Thegallstoneishandinglovewiththechronicliverinjuryandthelivercirrhosis.Rateofthegallstoneformationincreaseastheliverfunctiondecrease.Bacterialinfectionmaynotbethe0nlvfactorofthecholelithiasiswithchronicliverinjurys.[Keywords]Chronicliverinjures；Cholelithiasis；Uhrastructureofhepatocytes；Animalmodel近年，肝硬化后所引起的胆囊结石再次受到国内外学者的普遍关注。关于肝硬化合并胆囊结石的报道屡见不鲜.通过尸检、B超检查和临床资料回顾，国内肝硬化合并胆囊结样基金项目：广西自然科学基金项口（桂科自0640144）$通讯作者106巾国医药写报CHINAMEDICALHERALD石发病率为15.1％～59.0％l】21，其发病率至少为非肝硬化病人的两倍。有学者认为胆囊结石病伴随的肝脏损害，很可能是胆囊结石的成因，而不是后果，也许它先于胆囊结石而存在.而胆囊结石病的反复发作，反过来加重原发性肝损害『31。现对四氯~（CCL4）诱导的慢性肝损伤兔模型进行研究，报道如下：
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