异氟醚对大鼠缺血-再灌注损伤肝脏细胞黏附分子-1表达及中性粒细胞浸润的影响

目的 观察常温下异氟醚麻醉对大鼠部分肝脏缺血--再灌注(IR)损伤的影响,探讨异氟醚抗炎作用参与减轻肝脏IR损伤的可能机制.方法 雌性SD大鼠32只,随机均分为四组,A组,大鼠行腹腔注射1%戊巴比妥钠40mg/kg麻醉,进行手术但不阻断入肝血流;B组,1%戊巴比妥钠麻醉后行部分肝脏IR;C组,大鼠仅接受1.0 MAC异氟醚吸入麻醉,不阻断血流;D组,采用1.0 MAC异氟醚麻醉,并建立肝脏IR模型.肝脏IR损伤模型通过夹闭肝动脉和门静脉左支(支配肝左叶和中叶)建立,造成约70%肝脏缺血60min,再灌注3h,立刻取肝组织和血液标本.检测血清丙氨酸转氨酶(ALT)和天门冬氨酸转氨酶(AST)、肝组织内髓过氧化物酶(MPO)活性、肝组织细胞间黏附分子(ICAM-1)表达及肿瘤坏死因子α(TNF-α) mRNA转录水平,并进行HE染色行病理学检查.结果 B组血清ALT、AST水平和ICAM-1的表达、MPO活性明显高于A、C、D组(P<0.05),而D组明显高于A、C组(P<0.05);抑制肝脏再灌注后ICANI-1的表达以及MPO的活性(P<0.05).结论 异氟醚麻醉减轻肝脏IR损伤,可能与抑制ICANI-1和减少中性粒细胞(PMN)浸润有关.     

七氟醚对肢体缺血再灌注大鼠肝损伤的影响

目的探讨七氟醚对肢体缺血再灌注大鼠肝损伤的影响。方法健康SD大鼠24只,体重200～250g,随机分为3组,各8只:假手术组(Sham组),只进行手术操作不做其他处理;肢体缺血再灌注组(IR组),双后肢缺血4h、再灌注6h;七氟醚组(S组)于再灌注前吸入2.5%七氟醚6h。IR、Sham组只吸入氧气。实验结束断头处死大鼠,于下腔静脉取血测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)的含量。摘取肝脏测定肝组织匀浆超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)的含量,光学显微镜下观察组织病理学结果。结果与Sham组比较,IR组和S组ALT、AST、MDA、TNF-α和IL-6含量升高,SOD含量降低(P<0.01),肝组织损伤明显;与IR组比较,S组ALT、AST、MDA、TNF-α和IL-6含量降低,SOD含量升高(P<0.05),肝组织损伤减轻。结论七氟醚对肢体缺血再灌注大鼠肝损伤具有一定程度的保护作用,其机制可能与其减少氧自由基的释放和抑制炎症反应有关。     

ATP敏感性钾通道在硫化氢减轻大鼠肝缺血再灌注损伤中的作用

目的 评价ATP敏感性钾(KATP)通道在硫化氢减轻大鼠肝缺血再灌注损伤中的作用.方法 健康雄性SD大鼠30只,体重220～250 g,采用阻断左叶和中叶肝脏血流的方法制备肝缺血再灌注损伤模型.采用随机数字表法,将大鼠随机分为5组(n=6):假手术组(S组)仅开腹分离肝蒂,不进行肝门阻断及再灌注;缺血再灌注组(I/R组)制备肝缺血再灌注模型;硫氢化钠组(NaHS组)于再灌注前5 min时腹腔注射NaHS 28 μmol/kg,余同I/R组;格列本脲组(G组)于NaHS给药前5 min时腹腔注射非选择性KATP通道阻断剂格列本脲6 mg/kg,余同NaHS组;5-羟基葵酸组(5-HD组)于NaHS给药前5 min时腹腔注射选择性KATP通道阻断剂5-HD 10 mg/kg,余同NaHS组.于再灌注6h时,采集下腔静脉血样,测定血清ALT和AST的活性;然后处死大鼠,取肝组织,测定TNF-α含量和MPO活性,并观察病理学结果.结果 与S组比较,I/R组、NaHS组、G组和5-HD组血清ALT和AST活性升高,I/R组、G组和5-HD组肝组织TNF-α含量和MPO活性升高,NaHS组肝组织TNF-α含量升高(P＜0.01);与I/R组比较,NaHS组血清ALT、AST活性和肝组织TNF-α含量、MPO活性降低(P＜0.01),病理学损伤减轻;与NaHS组比较,G组和5-HD组血清ALT、AST活性和肝组织TNF-α含量、MPO活性升高(P＜0.01).结论 KATP通道的开放参与了硫化氢减轻大鼠肝缺血再灌注损伤.     

盐酸戊乙奎醚后处理对肢体缺血-再灌注大鼠肝损伤的影响

目的探讨盐酸戊乙奎醚对肢体缺血-再灌注大鼠肝损伤的影响。方法健康雄性Wistar大鼠108只,随机分为三组:对照组(C组)、肢体缺血-再灌注组(LIR组)及盐酸戊乙奎醚组(PHC组)。用弹力橡皮筋完全阻断大鼠双后肢血流3h,PHC组在缺血177min自尾静脉注射盐酸戊乙奎醚0.15mg/kg。三组分别在再灌注即刻(T0)、1h(T1)、3h(T2)、6h(T3)、12h(T4)、24h(T5)取血和肝组织,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)的活性,肿瘤坏死因子α(TNF-α)、白细胞介素10(IL-10)的浓度;检测肝组织丙二醛(MDA)含量及超氧化物歧化酶(SOD)、髓过氧化物酶(MPO)活性;光镜观察肝脏病理改变。结果 T3时LIR组及PHC组血清ALT、AST活性、肝脏组织MPO活性达到高峰;肝组织SOD活性最低,T1时血清TNF-α浓度达到高峰。与LIR组比较,T1～T3时PHC组血清ALT、AST活性下降,T1时血清TNF-α浓度下降,T1～T4时血清IL-10浓度升高,T1、T3时肝组织MDA含量降低,T1～T5时SOD活性升高,T1～T3时MPO活性下降(P<0.05)。光镜下,PHC组T3时肝组织病理学改变轻于LIR组。结论盐酸戊乙奎醚后处理对肢体缺血-再灌注大鼠肝脏具有一定保护作用,其机制可能与抑制活性氧生成及炎症反应有关。     

高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响

目的 探讨高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响.方法 雄性Wistar大鼠30只,体重300～350 g,随机分为3组(n=10):假手术组(S组)、缺血再灌注组(IR组)和高容量血液稀释组(HH组).S组仅开腹,不阻断血管;IR组阻断肝门静脉和左肝动脉30 min,再灌注2 h;HH组30 min内经尾静脉输注高渗氯化钠羟乙基淀粉40注射液10 ml/kg进行高容量血液稀释,输注完毕后15 min,行肝脏缺血再灌注.再灌注2 h时,下腔静脉取血样,测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性;取左肝叶组织,光镜下观察病理学结果,采用比色法测定丙二醛(MDA)含量,采用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性.结果 与S组比较,IR组和HH组血清ALT和AST的活性、肝组织MDA含量升高,肝组织SOD活性降低(P<0.01),肝组织病理学损伤明显;与IR组比较,HH组血清ALT和AST的活性、肝组织MDA含量降低,肝组织SOD活性升高(P<0.01),肝组织病理学损伤减轻.结论 高渗氯化钠羟乙基淀粉40注射液高容量血液稀释可减轻大鼠肝脏缺血再灌注损伤,可能与氧自由基生成减少有关.     

缺血后处理减轻肠缺血再灌注引起的肝损伤的机制研究

目的：探讨缺血后处理减轻肠缺血再灌注引起的肝损伤的作用机制,为外科防治缺血再灌注损伤提供策略。方法将36只SD大鼠随机分为假手术组（SO组,仅手术显露肠系膜上动脉）、缺血再灌注组（IR组,阻断肠系膜上动脉60min,再灌注120min）、缺血后处理组（IP组,阻断肠系膜上动脉60min后行3个循环的灌注30s/阻断30s,再持续灌注117min）,每组12只。建立模型2h后采集各组大鼠动、静脉血及部分小肠、肝组织,检测血肿瘤坏死因子α（TNF-α）、白细胞介素10（IL-10）、丙氨酸氨基转氨酶（ALT）、天门冬氨酸氨基转移酶（AST）水平,测定血清及肝组织内丙二醛（MDA）、髓过氧化酶（MPO）水平,光学显微镜下观察小肠及肝脏病理学改变,免疫组织化学法检测肝脏组织中核因子κBp65（NF-κBp65）和缺氧诱导因子1α（HIF-1α）的表达变化。结果与SO组比较,IR组小肠、肝脏病理损伤加重,肝组织NF-κBp65和HIF-1α的表达显著升高,血清和肝组织中MDA、MPO水平及血清TNF-α、IL-10、ALT和AST水平升高;与IR组比较,IP组小肠、肝脏损伤减轻,肝组织NF-κBp65表达下降而HIF-1α的表达显著升高,血清和肝组织中MDA、MPO水平及血清TNF-α、ALT和AST水平均显著下降,血清IL-10水平增加,差异均有统计学意义（P＜0.05）。结论缺血后处理可以促进抗炎因子的激活,抑制NF-κB信号通路调控的炎症级联反应,上调HIF-1α的表达,减轻小肠缺血再灌注引起的肝损伤。     

缺血预处理对肝脏缺血再灌注损伤中MPO、TNF-α、ET、NO的影响

目的：探讨缺血预处理（IPC）对肝脏缺血再灌注（I/R）损伤中的中性粒细胞和某些细胞因子的影响。方法：采用大鼠部分肝脏原位缺血再灌注损伤模型,30只Wistar大鼠随机分成：①正常对照组;②缺血再灌注对照组;③预处理组。②、③组均在60min再灌注完成后取血及肝组织标本,检测血清AST、ALT、LDH、NO、ET-1、TNF-α、及肝组织中髓过氧化酶（MPO）活性和肝细胞病理改变。结果：预处理组与再灌注对照组比较,肝功明显改善,NO含量升高,ET-1、TNF-α浓度和MPO活性明显降低,两组比较差异具有显著性。结论：缺血预处理对肝脏缺血再灌注损伤有明显保护作用,可能与提高内源性NO水平、减轻中性粒细胞在肝脏中的渗出和聚集、抑制ET-1、TNF-α的合成有关。     

异氟醚对大鼠肺缺血-再灌注损伤的影响

目的探讨异氟醚对大鼠肺缺血-再灌注损伤的影响.方法建立在体大鼠肺缺血-再灌注模型.120只SD雄性大鼠,随机分成四组：缺血-再灌注组（IR组）,异氟醚-缺血-再灌注组（ISO-IR组）,异氟醚组（ISO-C组）和手术对照组（C组）,每组30只.分别在缺血45 min、再灌注30、60、120 min处死大鼠行动脉血气分析、肺组织湿干比（W/D）值、丙二醛（MDA）含量及髓过氧化物酶（MPO）活性测定和肺组织病理学检查;此外,各组于再灌注120 min时另处死大鼠行支气管肺泡灌洗,取灌洗液（BALF）行白细胞计数、沉渣白细胞分类和BALF中总蛋白（TP）含量测定.结果再灌注后,IR组和ISO-IR组肺组织W/D值、MDA含量和MPO活性逐渐升高,且显著高于C组（P〈0.05）;但再灌注60 min后,ISO-IR组肺组织W/D值、MDA含量和MPO活性较IR组均有所降低（P〈0.05）.IR组BALF中的中性粒细胞（PMN）所占百分比较C组显著升高（P〈0.05）,而ISO-IR组的升高并不显著但较IR组显著降低;IR组和ISO-IR组BALF中TP含量均较C组显著升高（P〈0.05）,但ISO-IR组又低于IR组（P〈0.05）;肺组织病理学检查示ISO-IR组病理学变化较IR组显著减轻.结论异氟醚的吸入对缺血-再灌注损伤的肺组织具有一定的保护作用.     

七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤的保护作用

目的：探讨七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤的保护作用及其机制。方法：择期全麻下行右肝癌手术切除患者40例．ASAI或II级,术中经第一肝门阻断．血流阻断时间10～30min．随机分为2组（n=20）：缺血再灌注组（IR组）和七氟醚预处理组（S组）。两组麻醉维持期间均保持脑电双频谱指数40-50。s组麻醉诱导后吸入1MAC七氟醚（呼气末浓度）．30min后洗脱15min。于麻醉诱导前（T0）、缺血再灌注即刻（T1）、1h（T2）、6h（T3）抽血测血清中谷丙转氨酶（ALT）．谷草转氨酶（AST）,乳酸脱氢酶（LDH）的含量以及肝脏组织匀浆中丙二醛（MDA）含量和超氧化物岐化酶（SOD）活性,并行肝组织病理学观察。结果：与麻醉诱导前比较．两组缺血再灌注即刻．1h、6h血清ALT．AST,LDH含量均显著增加（P〈0．05）;与IR组比较,s组肝脏缺血再灌注后相应各时点血清ALT．AST、LDH含量均降低．肝组织匀浆MDA含量减少,SOD活性增加（P〈0．05）;肝组织病理学损伤减轻。结论：七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤有保护作用．可能与其抑制氧自由基生成．减少脂质过氧化有关。     

异氟醚对大鼠肺缺血再灌注损伤的保护作用

目的 探讨异氟醚对大鼠肺缺血再灌注损伤的保护作用。方法 120只SD雄性大鼠，随机分成4组（n=30）：假手术组（S组）、缺血再灌注组（IR组）、异氟醚-缺血再灌注组（ISO-IR组）和异氟醚组（ISO-S组）。IR组、ISO-IR组建立肺缺血再灌注模型，ISO-IR组吸入1MAC异氟醚30min时行肺缺血再灌注，ISO-S组吸入1MAC异氟醚，不进行肺缺血再灌注。分别在缺血45min、再灌注30、60、120min处死6只大鼠，测定肺组织湿干比（W／D）、髓过氧化物酶（MPO）活性、中性粒细胞（PMN）膜表面CD18和肺组织ICAM-1mRNA表达、支气管肺泡灌洗液（BALF）中自细胞计数、沉渣白细胞分类和总蛋白（TP）浓度，并进行肺组织病理学检查。结果 再灌注期间IR组肺组织W／D、MPO活性、CDl8和ICAM-1mRNA表达、BALF中PMN百分比、TP浓度及PMN膜表面CD18表达均升高。而异氟醚预先给药减弱了缺血再灌注诱导的上述指标的升高。肺组织病理学检查显示异氟醚预先给药减轻了肺缺血再灌注损伤。结论 通过抑制PMN浸润和肺组织ICAM-1mRNA及CD18表达上调，缺血前吸入异氟醚对肺缺血再灌注损伤有一定的保护作用。     

Genistein预处理对大鼠肝缺血再灌注损伤的保护作用

目的：探讨genistein预处理对肝脏缺血再灌注损伤的保护作用及其机制。
方法：54只SD大鼠完全随机分成3组。A组为I/R组:70%热缺血60 min及再灌注;B组为I/R
 genistein（GST）预处理组;C组为假手术组。于成模后2,6,12 h取大鼠血清和肝组织,检测血清AST,ALT浓度和肝组织MDA浓度,免疫组化法检测肝组织casepase-3蛋白的表达,光镜下观察肝脏组织病理变化。
结果：与I/R组相比,genistein预处理血清中AST及ALT浓度明显降低,肝组织病理损伤明显减轻。肝组织casepase-3蛋白表达及MDA浓度显著降低（均P＜0.05）。
结论：genistein预处理对大鼠肝脏热缺血再灌注具有保护作用,其机制与清除氧自由基,抑制细胞凋亡有关。     

Protection of preconditioning, postconditioning and combined therapy against hepatic ishemia/reperfusion injury

Objective： To study the protective effect of ischenlic preconditioning （I-pre） and ischemic postconditioning （I- post） against ischenlia/reperfusion （I/R） injury in rat＇ s liver. Methods： Using rat model of hepatic segmental I/R injury, rats were divided into 5 groups： Group A （sham group）, Group B （I/R injury）, Group C （I-pre group）, Group D （I-post group ） and Group E （combined treatment of I-pre and I-post ）. Serum alanine aminotransferase （ ALT ）, aspartate aminotransferase （ AST）, malondiaidehyde （ MDA ）, glutathione （ GSH ）, superoxide dismutase （ SOD ）, glutathione peroxidase （GSH-Px） and myeloperoxidase （MPO） in hepatic tissues were determined, respectively. In addition, 7 days＇survival of Groups B, C, D and E were evaluated. Results. Compared with Group B, Groups C, D and E exhibited significantly decreased ALT and AST release, minimized tissue injury, suppressed values of MDA and MPO, increased activities of SOD, GSH-Px and GSH （P〈0.05 ）, as well as improved animal survival. The differences among Groups C, D and E were not statistically significant. Conclusions： I-pre, I-post and combined therapy of I-pre and I-post have protective effect against hepatic I/R injury, which is correlated with its function of reducing the production of reactive oxygen species, maintaining the activities of antioxidant systems and suppressing neutrophils recruitment. No additive effect can be obtained in Group E.     

饮食中亚硝酸盐对大鼠肝缺血再灌注损伤的保护作用

目的 探讨饮食中亚硝酸盐对大鼠肝脏缺血再灌沣(I/R)损伤的保护作用.方法 Wistar 大鼠随机分为I/R组(对照组)、亚硝酸钠预处理组(实验组)和假手术组.建立大鼠肝脏部分I/R模型,实验组的饮水中加入少量亚硝酸盐并喂养7 d后建模,检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的水平,测定肝组织中超氧化物歧化酶(SOD),丙二醛(MDA),一氧化氮(NO),一氧化氮合酶(NOS)含量及活性.用Hoechst染色法检测细胞凋亡,并观察各组病理形态学的改变.结果 对照组AST,ALT,MDA水平和细胞凋亡的程度均明显异常.实验组上述指标的异常变化均明显减轻,NO明显高于对照组,差异有统计学意义(P＜0.01);但NOS并未增多,与对照组差异无统计学意义.结论 饮食中的亚硝酸盐对大鼠肝脏I/R损伤有明显的保护作用.     

Effect of Pharmacologic Preconditioning with Tetrandrine on Subsequent Ischemia/Reperfusion Injury in Rat Liver

The effect of tetrandrine (TET) pretreatment of Wistar rats subjected to warm hepatic ischemia/reperfusion (I/R) was investigated. After 50 minutes of ischemia in the left and median lobes of the liver and 24 hours of reperfusion (I/R group), the rats were killed. The TET+I/R group rats were pretreated with TET (50 mg/kg body weight IP) 30 minutes prior to the onset of ischemia. Blood samples were taken for measurement of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH). Tissue was taken from the ischemic lobes for measurement of superoxide dismutase (SOD), malonyldialdehyde (MDA), and myeloperoxidase (MPO); determination of the wet/dry weight (W/D) ratio; and histologic studies. The results showed that ALT, AST, and LDH levels in serum were increased in the I/R group; tissue MDA generation, MPO activity, and the W/D ratio were also increased, accompanied by decreased SOD activity. The serum ALT, AST, and LDH levels, as well as the tissue MPO level and W/D ratio, were lower in the TET+I/R group than in the I/R group; and the SOD level was higher in the TET+IR group than in the I/R group. Moreover, the serum ALT and AST, tissue MDA, and W/D ratio in the TET+I/R group were higher, and the SOD was lower than in the sham group. The histologic examination showed protection against liver damage in the TET+I/R group. The results demonstrated that pretreatment with TET could somewhat protect the liver against I/R injury but does not prevent it. The simultaneous decrease of both lipid peroxide generation and polymorphonuclear neutrophil infiltration in the ischemic liver may explain the acquisition of tolerance following administration of TET.     

Effect of Leptin and Apelin Preconditioning on Hepatic Ischemia Reperfusion Injury in Rats

Leptin and apelin are important adipocytokines involved in a variety of endocrine and paracrine functions. The aim of this study was to evaluate the effect of exogenous leptin and apelin preconditioning on hepatic ischemia reperfusion (I/R) injury in rats. Forty mice were assigned to four groups (n = 10): sham-operated control (sham), I/R injury, I/R + leptin (I/R + L), and I/R + apelin (I/R + A). Leptin 100 μg/kg/day and apelin 2 μg/kg/day were delivered intraperitoneally starting 3 days prior to surgical procedure in I/R + L and I/R + A groups, respectively. All I/R groups underwent 45 min of warm ischemia, followed by 30 min of reperfusion. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), liver malondialdehyde (MDA) and glutathione (GSH), and liver histopathology were compared between groups. MDA was elevated in I/R, but stayed similar in I/R + L and I/R + A compared to sham. I/R + A had significantly lower MDA compared to I/R. GSH levels did not differ significantly between the groups. ALT and AST were elevated in all I/R groups, but significant reduction was observed in I/R + L and I/R + A compared to I/R. Liver histopathology was mostly mild in I/R + L and I/R + A, in contrast to severe injury observed in the I/R group. Leptin and apelin preconditioning significantly reduced hepatic I/R injury in rats.     

The protective effect of aprotinin and alpha-tocopherol on ischemia-reperfusion injury of the rat liver

BACKGROUND: Liver injury caused by ischemia-reperfusion (I/R) processes is a complication of hepatic resection surgery and transplantation, particularly using grafts from marginal donors. Despite improvements in organ preservation and advances in surgical techniques, I/R injury remains a significant clinical problem. In this study, we investigated whether aprotinin provided protection against the adverse effects of I/R injury in liver tissue. METHODS: Forty rats were randomized into four groups (n = 10): group I: (control group) I/R + no medication; group II: sham-operated group + no medication or I/R; group III: I/R + aprotinin; group IV: I/R + alpha-tocopherol. Malondialdehyde (MDA) was measured in the liver tissue and superoxide dismutase (SOD), catalase (CAT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as lactate dehydrogenase (LDH) in rat serum. RESULTS: Administration of aprotinin and alpha-tocopherol before I/R resulted in significant reductions of MDA levels compared to the I/R alone group (group I; P = .01 and P < .01, respectively). Administration of aprotinin or alpha-tocopherol prior to I/R resulted in significant increases in SOD and CAT levels compared with the I/R group (P < .05 each). Compared to the I/R group, significant decreases in plasma AST, ALT, and LDH levels were observed both in the aprotinin and in the alpha-tocopherol group (P < .05). Histological evaluation revealed the injury grade to be relatively lower among groups III and IV compared to group I. DISCUSSION: In conclusion, rat hepatic structures in aprotinin and alpha-tocopherol administered groups were well protected. Therefore, aprotinin may provide protection against the adverse effects of I/R injury in liver transplantation.     

雌激素对大鼠肝切除肝缺血再灌注损伤中核因子-κB/IκB传导通路的影响及保护作用

目的 观察雌激素对大鼠肝切除肝缺血再灌注损伤中核因子-κB(NF-κB)/抑制蛋白(IκB)传导通路影响.方法 制作肝切除肝缺血再灌注损伤动物模型,雄性SD大鼠随机分为3组:假手术组(Sham组);肝切除肝缺血再灌注组(I/R组);肝切除肝缺血再灌注+雌激素组(I/R+ E2 组).分别在缺血再灌注后1、3、6h光镜下观察肝组织病理学改变,检测血清天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)的水平和肝组织丙二醛(MDA)的含量及超氧化物岐化酶(SOD)的活性,免疫组织化学法测定肝组织NF-κB的表达,Western blot检测NF-κB抑制蛋白(IκB-α)和细胞间黏附分子-1(ICAM-1)表达,流式细胞仪检测细胞凋亡率.结果 再灌注后I/R组在各时相血清ALT、AST均显著高于I/R +E2组,并于6h达到峰值(P＜0.05).与I/R+E2组和Sham比较,I/R组肝细胞凋亡率显著升高(P＜0.01);肝组织中IκB-α表达降低,而NF-κB表达增高(P＜0.05);ICAM-1 和MDA的结果变化和NF-κB表达水平变化类似,SOD呈相反变化.在光镜下观察,I/R组肝小叶结构紊乱,肝窦淤血,肝细胞水肿变性,肝细胞片状坏死,在Sham组和I/R +E2组上述病理学变化明显改善.结论 雌激素对肝切除肝脏缺血再灌注损伤有显著保护作用,其作用机制可能与雌激素影响NF-κB/IκB传导通路、减轻脂质过氧化反应、减少炎症介质释放及抑制细胞凋亡有关.     

瑞芬太尼对肝硬化大鼠肝脏缺血再灌注损伤的影响

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.