中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
7期
865-867
,共3页
井蕊%马万%马刚%王建珍%刘玉华
井蕊%馬萬%馬剛%王建珍%劉玉華
정예%마만%마강%왕건진%류옥화
哌啶类%再灌注损伤%肝%肝硬化,实验性
哌啶類%再灌註損傷%肝%肝硬化,實驗性
고정류%재관주손상%간%간경화,실험성
Piperidines%Reperfusion injury%Liver%Liver cirrhosis,experimental
目的 探讨瑞芬太尼对肝硬化大鼠肝脏缺血再灌注损伤的影响.方法 成年健康雄性SD大鼠30只,体重260~300 g,采用随机数字表法,将其随机分为3组(n=10):肝硬化组(C组)、肝硬化+肝缺血再灌注组(I/R组)和瑞芬太尼组(R组).C组、I/R组和R组采用四因素综合法制备大鼠肝硬化模型,I/R组和R组在肝硬化模型制备成功后1周制备大鼠70%肝脏缺血再灌注模型,R组于缺血前10 min开始静脉输注瑞芬太尼1μg·kg-1·min-至再灌注结束.于再灌注4h时取静脉血样和肝组织,测定血清ALT和AST活性、肝细胞Bcl-2和Bax表达及肝细胞凋亡情况,计算细胞凋亡指数,光镜下观察肝组织病理学结果.结果 与C组比较,I/R组血清ALT和AST的活性升高,肝细胞Bcl-2表达下调,Bax表达上调,细胞凋亡指数升高(P<0.05);与I/R组比较,R组血清ALT和AST的活性降低,肝细胞Bcl-2表达上调,Bax表达下调,细胞凋亡指数降低(P<0.05).R组肝组织病理学损伤轻于I/R组.结论 瑞芬太尼可减轻肝硬化大鼠肝脏缺血再灌注损伤,其机制与平衡肝细胞Bcl-2与Bax表达而抑制肝细胞凋亡有关.
目的 探討瑞芬太尼對肝硬化大鼠肝髒缺血再灌註損傷的影響.方法 成年健康雄性SD大鼠30隻,體重260~300 g,採用隨機數字錶法,將其隨機分為3組(n=10):肝硬化組(C組)、肝硬化+肝缺血再灌註組(I/R組)和瑞芬太尼組(R組).C組、I/R組和R組採用四因素綜閤法製備大鼠肝硬化模型,I/R組和R組在肝硬化模型製備成功後1週製備大鼠70%肝髒缺血再灌註模型,R組于缺血前10 min開始靜脈輸註瑞芬太尼1μg·kg-1·min-至再灌註結束.于再灌註4h時取靜脈血樣和肝組織,測定血清ALT和AST活性、肝細胞Bcl-2和Bax錶達及肝細胞凋亡情況,計算細胞凋亡指數,光鏡下觀察肝組織病理學結果.結果 與C組比較,I/R組血清ALT和AST的活性升高,肝細胞Bcl-2錶達下調,Bax錶達上調,細胞凋亡指數升高(P<0.05);與I/R組比較,R組血清ALT和AST的活性降低,肝細胞Bcl-2錶達上調,Bax錶達下調,細胞凋亡指數降低(P<0.05).R組肝組織病理學損傷輕于I/R組.結論 瑞芬太尼可減輕肝硬化大鼠肝髒缺血再灌註損傷,其機製與平衡肝細胞Bcl-2與Bax錶達而抑製肝細胞凋亡有關.
목적 탐토서분태니대간경화대서간장결혈재관주손상적영향.방법 성년건강웅성SD대서30지,체중260~300 g,채용수궤수자표법,장기수궤분위3조(n=10):간경화조(C조)、간경화+간결혈재관주조(I/R조)화서분태니조(R조).C조、I/R조화R조채용사인소종합법제비대서간경화모형,I/R조화R조재간경화모형제비성공후1주제비대서70%간장결혈재관주모형,R조우결혈전10 min개시정맥수주서분태니1μg·kg-1·min-지재관주결속.우재관주4h시취정맥혈양화간조직,측정혈청ALT화AST활성、간세포Bcl-2화Bax표체급간세포조망정황,계산세포조망지수,광경하관찰간조직병이학결과.결과 여C조비교,I/R조혈청ALT화AST적활성승고,간세포Bcl-2표체하조,Bax표체상조,세포조망지수승고(P<0.05);여I/R조비교,R조혈청ALT화AST적활성강저,간세포Bcl-2표체상조,Bax표체하조,세포조망지수강저(P<0.05).R조간조직병이학손상경우I/R조.결론 서분태니가감경간경화대서간장결혈재관주손상,기궤제여평형간세포Bcl-2여Bax표체이억제간세포조망유관.
Objective To investigate the effect of remifentanil on hepatic ischemia-reperfusion (I/R) injury in rats with liver cirrhosis.Methods Thirty male SD rats weighing 260-300 g were randomly divided into 3 groups (n =10 each):group liver cirrhosis (group C); group liver cirrhosis + hepatic I/R (group I/R) and group remifentanil (group R).Liver cirrhosis was produced in all animals in the 3 goups.I/R injury was induced by 20 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by 4 h reperfusion at 1 week after establishment of hepatic cirrhosis in I/R and R groups.In group R remifentanil was infused iv at 1 μg·kg-1 ·min-1 starting from 10 min before ischemia until the end of 4 h reperfusion.Venous blood samples were taken from inferior vena cava at the end of 4 h reperfusion for measurement of serum ALT and AST activities.The animals were then sacrificed and liver specimens were taken from middle lobe for determination of Bcl-2 and Bax expression (by immuno-histochemistry) and hepatocyte apoptosis (by TUNEL) and microscopic examination.Apoptosis index (percentage of apoptotic cells) was calculated.Results I/R significantly increased serum ALT and AST activities,Bax expression and apoptosis index and decreased Bcl-2 expression in group I/R as compared with group C.Remifentanil significantly attenuated the I/R-induced changes in serum ALT and AST activities,Bax and Bcl-2 expression and apoptosis in group R as compared with group I/R.Remifentanil also ameliorated I/R-induced liver damage.Conclusion Remifentanil can auenuate hepatic I/R injury in rats with liver cirrhosis by up-regulating Bcl-2 expression and down-regulating Bax expression and inhibiting apoptosis.