摘要
本研究以３０％ＩＩ°烧伤大鼠胃肠喂养模型，分离、培养枯否细胞，试图了解其在烧伤高代谢及伤后早期肠道营养中的作用。１０５只大鼠随机分为早期喂养组、延迟喂养组和正常对照组。于伤前及伤后１、３、５天动态观察血浆内毒素、代谢激素以及枯否细胞分泌ＴＮＦ、ＰＧＥ２的变化。还观察了伤后蛋白质代谢及肠道屏障功能的变化。结果表明延迟喂养组较早期喂养组肠粘膜屏障功能明显下降，血浆内毒素明显升高，分解激素升高而合成激素明显降低，空肠粘膜、腓肠肌含氮量均明显降低。作者认为，枯否细胞的过度激活可能是引发“肠源性高代谢”的重要环节之一。
ThisstudyaimedtoknowtherolesofKupfercelsinpostburncatabolism.Ratssus-tainedwith30%II°flameburnsofTBSAweredividedrandomlyintoearlyfeeding(EF)groupgivengastroenteralfeedingbeginningfrom2hourspostburn(n=45),anddelayedfeeding(DF)groupgiventhesamenutritionalsolutionsbutstartingonPBD3(=45).Another15ratswereservedasnormalcon-trols(NS)withoutburning.Theresultsshowedthatthebowel-barrier-functionreducedobviously,thethicknessofmucosaandheightofviliofjujunumdeclinedsignificantlyandtheplasmaendotoxinlevelwashigherintheDFgroupthanthatintheEFgroup.Therewereobviousincreaseofcatabolichormone(cortisol)levelanddecreaseofanabolichormone(insulin)levelinplasmaoftheDFgroupthanthatoftheEFgroup.Theproteincontentsofjejunummucosaandgastrocnemiusdecreasedsignificantly,TNFandPGE2releasedbyKCsalsoincreasedmoremarkedlyintheDFgroupthanthatintheEFgroup.Inconclusion.KCsmayplayoneofthekeyrolesinthe“gutderivedhypermetabolism”.Earlyenteralfeed-ingcanenhancethebarrierfunctionofintestinalmucosaandpreventthetranslocationofendotoxinfromguttobloodstreaminsomeextent.EarlyenteralfeedingcanreducecatabolismviathemodulationofhyperactivityofKCsandthedecreaseofexcessivesecretionofcatabolichormones.
出处
《中华外科杂志》
CAS
CSCD
北大核心
1996年第9期566-568,共3页
Chinese Journal of Surgery
