子痫前期模型大鼠下丘脑加压素表达的实验分析

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1、英文摘要AbstractAstudyonargininevasopressinexpressioninhypotha

2、amusofpreeclampsiaratsObjective：Thisstudywasaimedtoinvestigatethedistributionofargininevasopression(AVP)expressedpositiveneuronsinsupraoptienucleus(SON)andparaventricularnucleus(PVN)ofthepreeclampsiarats(PEgroup)，

3、normalpregnantrats(normalpregnantgroup)andhealthynon。pregnentrats(controlgroup)．Thesedataprovidemorphologicalevidencesforafurtherstudyofpathogenesisofpreeclampsia．Methods：(1)Weestablishedpre—eclampsiamodelbysubcutaneousinjectingNOsynthase(NOS)inhibitorN-Omega-Nitro—L-argi

4、ninemethylester(L-NAME)，andthehighermeanarterialpressure(MAP)andproteinuriameanssuccessfulmodeling．(2)Weobservedliverandrenalfunction，bodyweightofoffspringratsandplacentawetweightofmodelrats，andthencomparedwiththoseofnormalpregnantornon-pregnantrats．(3)Themorphologyanddis

5、tributionofAVPexpressedpositiveneuronswereobservedrespectivelyinSONandPVNofratsinthreegroupsbyusingimmunohistochemistrytechniqueinthesamesections．AllofthedatawereanalyzedbySAS8．0software．Results：(1)Thereweren0significantdifferencesintheMAPoftheratsamongallthegroupsbeforee

6、stablishingmodels．TheMAPand24一hrproteinuriaofpre—eclampsiagroupisstatisticallysignificantlyhigherthanthoseofnormalpregnantgroupandcontrolgroup(P2，3<0．05，Pl’3<0．05)．(2)ThereweresignificantdifferencesinthelevelofALT,AST,BUNandCrinratsamongmodelgroup，normalpregnantgroupandno

7、rmalnon-pregnantgroup(P

8、ofAVPpositiveneuronsinSONofpre-eclampsiaratsismuchmorethanthatofnormalpregnantgroupandcontrolgroup，anddifferenceofthenumberofAVPpositiveneuronsinSONhasstatisticalsignificance(P2，3<0．05，PL3<0．05)．Conclusion：(1)Thepreeclampsiamodelratscouldcausenotonlytheseriouspathological

9、chan-gesinliverandotherimportantorgans，butalsoworseoffspringoutcomesofintrauterinegrowthrestrict