国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2013年
8期
707-710,719
,共5页
依达拉奉%体外循环%转化生长因子-β1%肺损伤%犬
依達拉奉%體外循環%轉化生長因子-β1%肺損傷%犬
의체랍봉%체외순배%전화생장인자-β1%폐손상%견
Edaravone%Transforming growth factor-β1%Cardiopulmonary bypass%Lung injury%Dog
目的 观察依达拉奉(edaravone,ED)对体外循环(cardio-pulmonary bypass,CPB)犬肺组织转化生长因子-β1(transforming growth factor-β1,TGF-β1)的影响. 方法 建立成年犬CPB相关肺损伤模型,随机双盲分为3组(每组10只):C 组(CPB中用生理盐水),E1组(CPB前用ED),E2组(CPB中用ED).检测CPB前(T0)、CPB中30 min (T1)、停机后15(T2)、30(T3)、60 min(T4)肺组织超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量及TGF-β1表达,采用光镜观察肺组织病理结构,同时于T0、T3、T4时抽取动脉血测定呼吸指数(respiratory index,RI). 结果 与T0比较,T3、T4时间点3组RI均升高(P<0.05),E1组、E2组升高[(1.21±0.39),(1.33±0.51);(1.87±0.53),(2.31±0.67)]幅度低于C组[(4.66±0.71),(5.19±0.43)(P<0.05)],且E1组低于E2组(P<0.05).各组在T1~T4时肺组织中SOD活性均下降(P<0.05);E1组[(10.2±1.1)、(9.9±1.5)、(9.8±1.1)、(10.2±1.1) U/mg]、E2组[(10.4±1.2)、(10.0±1.1)、(9.9±1.2)、(10.2±1.1) U/mg],在T1~T4时SOD活性高于C组[(8.4±1.2)、(8.1±1.7)、(8.0±1.2)、(8.3±1.3) U/mg] (P<0.05).各组在T1~T4时肺组织MDA含量均升高(P<0.05);E1组、E2组在T~1T4时MDA含量低于C组(P<0.05).组织学检查:C组肺部炎症反应较重;E1组、E2组炎症反应较轻;T0时3组肺组织中偶见TGF-β1表达;T1~T4时各组肺组织中TGFβ-1表达均增强,且E1组[(169.6±1.1),(183.9±1.1),(173.8±0.9),(186.0±0.7)]弱于E2组[(150.4±1.1),(166.2±1.0),(151.7±0.8),(153.2±0.8)]、C组[(143.2±1.2),(140.3±0.8),(133.3±0.7),(146.4±0.8)](P<0.05). 结论 CPB增强肺组织TGF-β1表达,加重肺损伤,ED能抑制肺组织TGF-β1表达,减轻肺损伤.CPB前使用ED的保护效果优于在CPB过程中使用.
目的 觀察依達拉奉(edaravone,ED)對體外循環(cardio-pulmonary bypass,CPB)犬肺組織轉化生長因子-β1(transforming growth factor-β1,TGF-β1)的影響. 方法 建立成年犬CPB相關肺損傷模型,隨機雙盲分為3組(每組10隻):C 組(CPB中用生理鹽水),E1組(CPB前用ED),E2組(CPB中用ED).檢測CPB前(T0)、CPB中30 min (T1)、停機後15(T2)、30(T3)、60 min(T4)肺組織超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量及TGF-β1錶達,採用光鏡觀察肺組織病理結構,同時于T0、T3、T4時抽取動脈血測定呼吸指數(respiratory index,RI). 結果 與T0比較,T3、T4時間點3組RI均升高(P<0.05),E1組、E2組升高[(1.21±0.39),(1.33±0.51);(1.87±0.53),(2.31±0.67)]幅度低于C組[(4.66±0.71),(5.19±0.43)(P<0.05)],且E1組低于E2組(P<0.05).各組在T1~T4時肺組織中SOD活性均下降(P<0.05);E1組[(10.2±1.1)、(9.9±1.5)、(9.8±1.1)、(10.2±1.1) U/mg]、E2組[(10.4±1.2)、(10.0±1.1)、(9.9±1.2)、(10.2±1.1) U/mg],在T1~T4時SOD活性高于C組[(8.4±1.2)、(8.1±1.7)、(8.0±1.2)、(8.3±1.3) U/mg] (P<0.05).各組在T1~T4時肺組織MDA含量均升高(P<0.05);E1組、E2組在T~1T4時MDA含量低于C組(P<0.05).組織學檢查:C組肺部炎癥反應較重;E1組、E2組炎癥反應較輕;T0時3組肺組織中偶見TGF-β1錶達;T1~T4時各組肺組織中TGFβ-1錶達均增彊,且E1組[(169.6±1.1),(183.9±1.1),(173.8±0.9),(186.0±0.7)]弱于E2組[(150.4±1.1),(166.2±1.0),(151.7±0.8),(153.2±0.8)]、C組[(143.2±1.2),(140.3±0.8),(133.3±0.7),(146.4±0.8)](P<0.05). 結論 CPB增彊肺組織TGF-β1錶達,加重肺損傷,ED能抑製肺組織TGF-β1錶達,減輕肺損傷.CPB前使用ED的保護效果優于在CPB過程中使用.
목적 관찰의체랍봉(edaravone,ED)대체외순배(cardio-pulmonary bypass,CPB)견폐조직전화생장인자-β1(transforming growth factor-β1,TGF-β1)적영향. 방법 건립성년견CPB상관폐손상모형,수궤쌍맹분위3조(매조10지):C 조(CPB중용생리염수),E1조(CPB전용ED),E2조(CPB중용ED).검측CPB전(T0)、CPB중30 min (T1)、정궤후15(T2)、30(T3)、60 min(T4)폐조직초양화물기화매(superoxide dismutase,SOD)활성、병이철(malondialdehyde,MDA)함량급TGF-β1표체,채용광경관찰폐조직병리결구,동시우T0、T3、T4시추취동맥혈측정호흡지수(respiratory index,RI). 결과 여T0비교,T3、T4시간점3조RI균승고(P<0.05),E1조、E2조승고[(1.21±0.39),(1.33±0.51);(1.87±0.53),(2.31±0.67)]폭도저우C조[(4.66±0.71),(5.19±0.43)(P<0.05)],차E1조저우E2조(P<0.05).각조재T1~T4시폐조직중SOD활성균하강(P<0.05);E1조[(10.2±1.1)、(9.9±1.5)、(9.8±1.1)、(10.2±1.1) U/mg]、E2조[(10.4±1.2)、(10.0±1.1)、(9.9±1.2)、(10.2±1.1) U/mg],재T1~T4시SOD활성고우C조[(8.4±1.2)、(8.1±1.7)、(8.0±1.2)、(8.3±1.3) U/mg] (P<0.05).각조재T1~T4시폐조직MDA함량균승고(P<0.05);E1조、E2조재T~1T4시MDA함량저우C조(P<0.05).조직학검사:C조폐부염증반응교중;E1조、E2조염증반응교경;T0시3조폐조직중우견TGF-β1표체;T1~T4시각조폐조직중TGFβ-1표체균증강,차E1조[(169.6±1.1),(183.9±1.1),(173.8±0.9),(186.0±0.7)]약우E2조[(150.4±1.1),(166.2±1.0),(151.7±0.8),(153.2±0.8)]、C조[(143.2±1.2),(140.3±0.8),(133.3±0.7),(146.4±0.8)](P<0.05). 결론 CPB증강폐조직TGF-β1표체,가중폐손상,ED능억제폐조직TGF-β1표체,감경폐손상.CPB전사용ED적보호효과우우재CPB과정중사용.
Objective To study the effects of edaravone (ED) on the expression of lung transforming growth factor-β1 (TGF-β1) in dogs with cardio-pulmonary bypass (CPB).Methods Thirty adult dogs were randomly divided into three groups (n =10):group C receiving normal saline during CPB,group E1 receiving ED before CPB,and group E2 receiving ED during CPB.Lung superoxide dismutase (SOD) activity,malondialdehyde (MDA) level,and TGF-β1 expression were determined before CPB (T0),30 min during CPB (T1),15 rmin after CPB (T2),30 min after CPB (T3),60 min after CPB (T4) in all dogs.The histological pathology of lung was evaluated with light microscope.Arterial blood samples were collected for the monitoring of respiratory index (RI) at T0,T3 and T4.Results Compared with T0,RI increased at T3 and T4 in all groups(P<0.05).RI was higher in group C [(4.66±0.71),(5.19±0.43)] than group E1 [(1.21±0.39),(1.33±0.51)] or E2 [(1.87±0.53),(2.31±0.67)] and was higher in group E2 than group E1(P<0.05).Compared with T0,SOD activity decreased gradually at T1-T4 in all groups (P<0.05).SOD activity was higher in groups E1[(10.2±1.1),(9.9±1.5),(9.8±1.1),(10.2±1.1) U/mg] and E2 [(10.4±1.2),(10.0±1.1),(9.9±1.2),(10.2±1.1) U/mg] than group C[(8.4±1.2),(8.1±1.7),(8.0±1.2),(8.3±1.3) U/mg] at T1-T4 (P<0.05).Compared with T0,MDA level increased gradually at T1-T4 (P<0.05).MDA level was lower in groups E1 and E2 than group C at T1-T4(P<0.05).Histopathological observation:group C showed severe inflammatory responses that were alleviated in groups E1 and E2.The expression of TGF-β1 was ocassionally detected at T0,and increased at T1-T4 in all groups.TGF-β1 expression was lower in group E1 [(169.6±1.1),(183.9±1.1),(173.8±0.9),(186.0±0.7)] than groups E2 [(150.4±1.1),(166.2±1.0),(151.7±0.8),(153.2±0.8)] and C [(143.2±1.2),(140.3±0.8),(133.3±0.7),(146.4±0.8)](P<0.05).Conclusions CPB increased lung TGF-β1 expression and injury,which might be improved by ED.ED used before CPB provided better protection than used during CPB.