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1、Chinese3ournaf0fNeWDrugs2010，19(22)鹽酸戊乙奎醚對創(chuàng)傷失血性休克復蘇后大鼠急性肺損傷的影響趙子松，張良成，周琳瑛(1福州市第二醫(yī)院麻醉科，福州350007；2福建醫(yī)科大學附屬協(xié)和醫(yī)院麻醉科，福州350001；3福建醫(yī)科大學電子顯微鏡室，福州350004)[摘要]目的：探討鹽酸戊乙奎醚對大鼠創(chuàng)傷失血性休克復蘇后肺組織急性炎性損傷的影響。方法：制作創(chuàng)傷失血性休克大鼠模型，取各組大鼠的肺組織標本，測定肺組織濕／干重比，光鏡下觀察肺組織形態(tài)學損傷情況，免疫組織化學和WesternBlot方
2、法半定量分析TNF—，核轉錄因子．KB(NF—KB)、抑制因子．KB(I-KB)的表達情況。結果：與空白對照(S)組比較，模型對照(R1)、鹽酸戊乙奎醚治療(R2)組的肺濕／干重比和TNF一表達顯著增高(P<0．01)，胞漿I-KB明顯降解(P<0．05)，NF—KB向細胞核內轉移明顯；R2組與R1組比較，肺組織濕／干重比顯著降低(P<0．05)，炎癥細胞浸潤和水腫程度均較R1組有所改善，TNF—的胞漿表達也較R1組低(P<0．05)；NF—KB向胞核轉移較R1組明顯減少；WesternBlot蛋白半定量分析可見R
3、2組胞漿I-KB的含量較高，表明降解減少(P<0．05)。結論：復蘇早期應用鹽酸戊乙奎醚治療，可明顯減輕急性肺損傷程度。[關鍵詞]休克／創(chuàng)傷失血性；急性肺損傷；核轉錄因子．KB；鹽酸戊乙奎醚[中圖分類號]R971．2[文獻標志碼]A[文章編號]1003—3734(2010)22—2085—05Effectofpenehyclidinehydr0chlorideonacutelunginjuryfollowingtrauma／hemorrhagicshockandresuscitationinratsZHA0Zi—s
4、ong，ZHANGLiang—cheng，ZHOULin—ying(1DepartmentofAnesthesiology，TheSecondHospitalofFuzhou，F(xiàn)uzhou350007，China；2DepartmentofAnesthesiology，TheAffiliatedUnionHospitalofFujianMedicalUniversity，F(xiàn)uzhou350001，China；3DivisionofElectronMicroscopy，F(xiàn)ujianMedicalUniversity，
5、Fuzhou350004，China)[Abstract]objective：Toinvestigatetheeffectofpenehyclidinehydrochlorideonacuteinflammatoryinju—riesfollowingtrauma／hemorrhagicshockandresuscitationinrats．Methods：Afterthemodeloftrauma／hemorrhag-icshockandresuscitationwasestablished，lungtissue
6、sweregathered．Wetanddryweightsofthelungtissueweremeasuredandthewet／dryratiowascalculated；morphologicalchangeswereobservedunderlightmicroscope；theexpressionofTNF—andthetranslocationofNF—KBfromthecytoplasmtothenucleuswereevaluatedbyimmuno—histochemicalstaining；t
7、helevelofI-KBinthecytoplasmwasmeasuredbyWesternblotting．Results：Noinflam—matorydamagewasfoundinlungsofratsincontrolgroup．Wet／dryratiooflungtissues，theinfiltrationofinflam—matorycellsandthethicknessofwallofalveoliinlungswereincreased(P<0．01)aftertrauma／hemorrha
8、gicshockandresuscitation．However，theseincreasesinpenehyclidinegroupweresignificantlymoreslightthanthoseinmodelgroup(P<0．05)．ThechangesinTNF一僅expression，I-KBdegenerationofandNF—KBtr
