七氟醚对大鼠急性肾缺血-再灌注损伤的保护作用

目的探讨七氟醚对急性肾缺血-再灌注损伤的保护作用及其机制。方法SD大鼠18只,随机均分为缺血-再灌注组(I/R组)、七氟醚组(S组)和对照组(C组)。建立大鼠急性肾缺血-再灌注损伤模型,缺血-再灌注后3h分别检测血清尿素氮(BUN)、肌酐(Cr)、超氧化物歧化酶(SOD)、丙二醛(MDA)及观察肾组织的病理学变化。结果与C组比较,I/R组和S组血清BUN、Cr水平显著增加(P<0.05),但S组BUN、Cr低于I/R组(P<0.05)。与I/R组比较,S组SOD显著升高,MDA显著降低(P<0.05)。S组肾组织病理损伤分级明显低于I/R组(P<0.05)。结论七氟醚对大鼠急性肾缺血-再灌注损伤具有保护作用,抑制氧自由基反应可能是其重要机制。     

七氟醚预处理对大鼠肾缺血再灌注损伤的影响

目的 评价七氟醚预处理对大鼠肾缺血再灌注损伤的影响.方法 雄性SD大鼠24只,体重250～300 g,采用随机数字表法,将大鼠随机分为3组(n=8):假手术组(S组)、肾缺血再灌注组(I/R组)和七氟醚预处理组(SP组).I/R组和SP组采用切除右肾然后夹闭左侧肾动脉45 min再开放的方法 制备肾缺血再灌注模型.SP组吸入2.2%七氟醚1 h,停止吸入后10 min时进行肾缺血.于再灌注2 h时采集静脉血样,测定血清肌酐(Cr)、尿素氮(BUN)和胱抑素C(Cys C)的浓度,取肾组织,光镜下及透射电镜下观察病理学结果,并根据肾小管病变程度进行Paller评分.结果 与S组比较,I/R组血清Cr和BUN浓度差异无统计学意义(P＞0.05),血清Cys C浓度和Paller评分明显升高(P＜0.05);与I/R组比较,SP组血清Cys C浓度和Paller评分明显降低(P＜0.05).SP组肾组织损伤程度轻于I/R组.结论 七氟醚预处理可减轻大鼠肾缺血再灌注损伤.

Abstract：

Objective To investigate the effects of sevoflurane preconditioning on renal ischemia-reperfusion(I/R)injury in rats.Methods Twenty-four adult male SD rats weighing 250-300 g were randomly divided into 3 groups(n=8 each):sham operation group (group S);I/R group; sevoflurane preconditioning group (group SP). After the rats underwent right nephrectomy, renal I/R was produced by occlusion of left renal artery for 45 min followed by reperfusion in I/R and SP groups.In group SP, the rats inhaled 2.2% sevoflurane for 1 h, then the inhalation was stopped and renal ischemia was performed 10 min later. Venous blood samples were collected at 2 h of reperfusion to determine the concentrations of serum creatinine(Cr), urea nitrogen (BUN), cystatin C (Cys C) . The renal tissues were obtained for microscopic examination, and Paller's score was recorded. Results Compared with group S, there was no significant difference in the serum Cr and BUN concentrations (P＞0.05), while the serum Cys C concentration and Paller's score for acute renal tubular injury were significantly increased in group I/R(P＜0.05). The serum Cys C concentration and Paller's score were significantly lower in group SP than in group I/R(P＜0.05).I/R-induced renal injury was significantly reduced in group SP compared with group I/R. Conclusion Preconditioning with sevoflurane can provide significant protection against renal I/R injury.     

七氟醚对肺缺血／再灌注损伤的保护机制

背景七氟醚作为一种较理想的吸入麻醉药,被广泛应用于临床,实验表明七氟醚对肺缺血／再灌注损伤（ischemia／reperfusion injury,I／RI）具有保护作用。目的通过分析近年的研究总结七氟醚对肺I／RI的保护机制。内容七氟醚通过减轻肺通透性、抑制炎症反应、减轻脂质过氧化反应、抑制细胞凋亡、减轻细胞内钙离子超载等发挥肺I／RI的保护作用。趋势应进一步探讨七氟醚对肺的保护作用,加强对七氟醚的临床应用研究,为实际临床工作提供可靠的依据。     

异氟醚预处理对大鼠肝脏缺血再灌注损伤的影响

目的 探讨异氟醚预处理对大鼠肝脏缺血再灌注损伤的影响.方法 成年雄性SD大鼠24只,体重180～220 g,随机分为3组(n=8):假手术组(S组)吸人纯氧30 min,间隔30 min后仅开腹;肝脏缺血再灌注组(IR组)吸入纯氧30 min,间隔30 min后行肝脏缺血60 min,再灌注4 h;异氟醚预处理组(Iso组)吸入1.4%异氟醚30 min,间隔30 min后行肝脏缺血60 min,再灌注4 h.于再灌注4 h时处死大鼠,留取肝脏及腹主动脉血5ml.测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)浓度,血清及肝组织匀浆上清液中肿瘤坏死因子α(TNF-α)的浓度,肝组织髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,观察肝组织病理学改变.结果 与S组比较,IR组、Iso组血清ALT、AST和TNF-α水平明显升高,肝组织TNF-α含量升高,肝组织MPO活性升高,MDA含量升高,SOD活性降低(P＜0.05或0.01),肝组织病理损伤明显;与IR组比较,Iso组血清ALT、AST和TNF-α水平降低,肝组织TNF-α含量降低,肝组织MPO活性降低,MDA含量降低,SOD活性升高(P＜0.05或0.01),肝组织病理损伤程度减轻.结论 1.4%异氟醚预处理可明显减轻大鼠肝脏缺血再灌注损伤,其机制可能与抑制TNF-α的释放、减少中性粒细胞在肝组织的浸润有关.     

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。     

肝脏缺血再灌注损伤机制和缺血预处理保护作用

缺血再灌注(ischemia reperfusion, IR)损伤是指缺氧器官细胞损伤在恢复氧供之后更加加重的现象。Toledo Pereyra 等在 1975 年首先认识到IR损伤是肝移植过程中一种重要病理损伤状态,可发生移植肝淤血、进行性血栓形成和/或器官坏死,导致移植失败。直到80年代中期,“再灌注损伤(reperfusion injury)”才逐渐在肝移植文献中应用。　　肝脏IR损伤可分为热缺血和冷保存缺血再灌注损伤。热 IR 损伤(warm ischemia reperfu sion injury)与肝脏外科、肝移植、低血容量性休克、毒性肝损害、静脉阻塞性疾病和 Budd Chiari综合征等普遍相关…     

七氟醚对在体大鼠肺缺血-再灌注损伤的影响

目的研究七氟醚对在体大鼠肺缺血-再灌注(I-R)损伤的影响。方法40只Wistar大鼠建立在体大鼠肺I-R模型,随机分为四组,每组10只:A组,假手术组,开胸后机械通气120 min;B组,I-R组,阻断左肺门60 min,开放再通气60 min;C组,七氟醚加I-R组,缺血前吸入1 MAC七氟醚30 min,开放再通气同时吸入1 MAC七氟醚60 min;D组,七氟醚组,持续吸入1 MAC七氟醚120min。观察各组实验结束时肺组织的湿/干重比(W/D)、肺丙二醛(MDA)、超氧化物歧化酶(SOD)和肺组织病理学的改变。结果B组及C组肺W/D较A组和D组显著升高(P<0.01,P<0.05),SOD含量显著低于A组和D组(P<0.05);B组肺MDA含量较A组和D组显著升高(P<0.01),C组肺MDA含量较B组低(P<0.05);C组肺W/D、肺MDA显著低于B组(P<0.05),SOD高于B组(P<0.05);病理切片见B组、C组部分肺泡结构破坏,肺泡间隔增宽,肺泡腔内水肿并有出血,以B组改变较为严重,炎症积分显著高于C组(P<0.01)。结论七氟醚对在体大鼠肺I-R损伤有一定的保护作用。     

七氟醚预处理对肝脏缺血-再灌注损伤及PI3K/Akt信号通路的影响

目的 探讨七氟醚预处理对肝脏缺血-再灌注损伤及磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号通路的影响.方法 48只成年SD大鼠随机分为假手术组(SH组)、缺血-再灌注组(IR组)、七氟醚预处理组(SI组)和七氟醚Wortmannin组(SW组),每组12只.除SH组外,IR组、SI组和SW组建立70％肝脏缺血-再灌注模型.检测大鼠血清谷草转氨酶(AST)和谷丙转氨酶( ALT)含量,并取再灌注的肝组织用ELISA法测IL-1β浓度,用Western Blot法测定肝组织的p-PI3K、p-Akt(ser473)、Akt等表达量;用HE染色进行病理学检查,观察肝细胞损伤及坏死情况.结果 与SW组比较,SI组ALT、AST和IL-1β浓度明显降低(P＜0.05),且p-PI3K、p-Akt(ser473)表达量明显增加(P＜0.05),肝组织损伤减轻.结论 七氟醚对肝脏缺血-再灌注损伤有保护作用,可能通过激活PI3K/Akt信号通路起作用.     

一氧化氮在七氟醚预处理减轻兔心肌缺血再灌注损伤中的作用

目的 评价一氧化氮在七氟醚预处理减轻兔心肌缺血再灌注损伤中的作用.方法 健康雄性新西兰大白兔40只,体重2.1～2.9 kg,随机分为5组(n=8):缺血再灌注组(IR组)、七氟醚预处理组(SEV组)、L-NAME组、七氟醚预处理+L-NAME组(SL组)和L-NAME+七氟醚预处理组(LS组).采用结扎冠状动脉前降支45 min,再灌注3 h的方法制备兔心肌缺血再灌注模型.SEV组吸入1.7%七氟醚30 min,洗脱15 min行预处理后制备模型;L-NAME组静脉注射一氧化氮合酶(NOS)抑制剂L-NAME 1 mg/kg,5 min后制备模型;SL组七氟醚预处理后,静脉注射L-NAME 1 mg/kg,5 min后制备模型;LS组静脉注射L-NAME 1 mg/kg,5 min后行七氟醚顶处理,制备模型.于模型制备前即刻(T0)、心肌缺血45 min(T1)、再灌注60 min(T2)、120 min(T3)、180 min(T4)时记录HR、MAP、左室收缩压(LVSP)和左室收缩压最大上升速率(+dp/dtmax),于T4时抽取股动脉血3 ml,测定血浆心肌肌钙蛋白T(cTnT)浓度、心肌磷酸肌酸激酶(CK-MB)和乳酸脱氢酶(LDH)活性,取心室肌组织,测定心肌缺血危险区(AAR)和梗塞区(IS)面积,并计算IS/AAR.结果 与IR组比较,SEV组缺血再灌注时+dp/dtmax升高,血浆cTnT浓度、CK-MB和LDH活性和心室肌IS/AAR降低(P<0.05),其余组上述指标差异均无统计学意义(P0.05).结论 一氧化氮参与了七氟醚预处理减轻兔心肌缺血再灌注损伤,一氧化氮可能是其保护作用中某一通路上的信号分子.     

七氟醚和安氟醚对心肌缺血再灌注损伤的保护作用

目的：从细胞生化方面来探讨七氟醚和安氟醚对心肌缺血再灌注损伤的影响。方法：采用Ｌａｎｇｅｎｄｏｒｆ离体大鼠心脏模型，将３０只大鼠随机分成三组：对照组、七氟醚组和安氟醚组，每组各１０只。全心缺血３０分钟，再灌注３０分钟。结果：缺血前给予１ＭＡＣ的七氟醚或安氟醚可以明显减少再灌注冠脉流出液中乳酸脱氢酶和蛋白的释放量，降低心肌细胞内钙聚集，保护了心肌ＳＯＤ的活力。结论：七氟醚和安氟醚对缺血再灌注心肌有显著的保护作用。     

缺血预处理对大鼠肝脏低温保存损伤的保护作用

目的　探讨缺血预处理 (IPC)对大鼠肝脏低温保存损伤的保护作用。方法　制备大鼠肝脏离体非循环灌注模型 ,对供肝分别作不同时间的IPC (IPC1组缺血 5min、IPC2 组缺血 10min、IPC3 组缺血 15min) ,而后比较各组供肝的损伤程度。结果　流出液中AST和ALT的水平 ,IPC1组分别为 (4 0 .1± 6.3 )U/L和 (17.1± 0 .5 )U /L ,IPC2 组分别为 (5 3 .6± 3 .7)U/L和 (19.7± 0 .5 )U /L ,均显著低于未预处理 (NPC)组的 (64 .5± 8.2 )U/L和 (2 3 .8± 3 .9)U /L (P<0 .0 5 ) ;IPC1组又显著低于IPC2 组和IPC3 组的 (63 .8± 7.2 )U/L和 (2 2 .8± 2 .5 )U /L (P<0 .0 5 )。LDH水平 ,NPC组、IPC1组、IPC2 组和IPC3 组分别为 (10 4.3± 2 0 .6)U/L、(84.1± 19.7)U /L、(90 .5± 2 1.1)U/L和 (10 3 .1± 18.5 )U /L ,4组间差异无统计学意义 (P>0 .0 5 ) ,但均高于正常组〔(71.5± 18.9)U /L〕 (P<0 .0 5 )。胆汁分泌量及肝组织ATP含量 ,IPC1组分别为 (5 3 .5± 10 .2 ) μl和 (6.15± 0 .65 ) μmol/g ,IPC2 组分别为 (4 1.5± 8.1) μl和 (4 .77± 0 .2 1) μmol/g ,均显著高于NPC组的 (2 2 .8± 9.7) μl和 (2 .62± 0 .3 4) μmol/g (P<0 .0 5 ) ;IPC1组又显著高于IPC2 组和IPC3 组的 (2 7.5± 2 .8) μl和 (2 .61     

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.     

一氧化氮在大鼠肝脏缺血预处理中的作用

为探讨ＮＯ是否参与缺血预处理对肝脏的保护作用，本实验将动物分成四组：①正常对照组，不作肝门阻断；②再灌对照组：肝脏进行６０分钟的肝门阻断及３０分钟的再灌注；③预处理组：６０分钟的肝门阻断前先进行５分钟的肝脏缺血及５分钟的再灌注；④预处理加Ｌ－ＮＮＡ（Ｐ＋Ｌ）组：在预处理前先经门静脉注射Ｌ－ＮＮＡ。各组均在３０分钟再灌注完成时取肝组织标本及血标本检查ＡＴＰ、肝功能、脂质过氧化产物。结果显示：经过６０分钟的缺血及３０分钟的再灌注后，再灌对照组肝功能明显受损、ＡＴＰ浓度下降、脂质过氧化产物增加。预处理则能明显改善肝功能、增加ＡＴＰ储备和减少脂质过氧化。Ｐ＋Ｌ组则与再灌对照组无显著差异。结果表明：ＮＯ合成抑制剂Ｌ－ＮＮＡ能阻断缺血预处理对肝脏缺血再灌注损伤的保护作用，说明ＮＯ参与大鼠肝脏缺血预处理     

缺血预处理对大鼠移植肝脏缺血再灌注损伤的保护作用

目的　探讨缺血预处理 (ischemicpreconditioning ,IP)对大鼠移植肝脏缺血再灌注损伤的保护作用。 方法　采用SD大鼠原位肝移植动物模型 ,供肝冷保存时间 10 0min ,无肝期 2 5min。 64只SD大鼠随机均分成两组 :对照组 ,获取供肝前仅以肝素生理盐水经门静脉灌注 ;IP组 ,获取供肝前阻断肝门血供 10min ,再灌注 10min ,然后再以肝素生理盐水经门静脉灌注。每组受体的一半 (n =8)用于观察存活率 ,另一半 (n =8)用于移植肝脏再灌注 2h后取血及肝脏检测。结果　IP组的 1w存活率、胆汁分泌量、抗氧化酶活力、血清NO水平均明显高于对照组 (P<0 .0 5 ) ,血清ALT、AST、LDH、TNF及肝组织中的过氧化产物含量均明显低于对照组 (P<0 .0 5 ) ,组织的病理改变也轻于对照组。结论　IP能够提高血清NO水平 ,降低血清TNF含量 ,对大鼠移植肝脏的缺血再灌注损伤具有保护作用     

人参皂甙Rb1对肺缺血再灌注损伤的保护作用

目的探讨人参皂甙Ｒｂ１对肺缺血再灌注损伤的保护作用。方法按肺移植供肺获取和保存的方法，对３５只家兔的肺分别获取，保存；然后采用体外装置，建立体外肺缺血再灌注损伤模型。在即将再灌流前，将不同剂量的Ｒｂ１加入到５０ｍｌ再灌流血液中。结果Ｒｂ１可使肺组织中超氧化物歧化酶（ＳＯＤ）含量升高，丙二醛（ＭＤＡ）含量降低；使肺动脉压（ＰＡＰ）降低，湿肺干肺比重降低和改善肺组织病理变化。Ｒｂ１在再灌流血液中浓度为８０ｍｇ／Ｌ时，已有明显效果。结论Ｒｂ１对肺缺血再灌注损伤具有明显的保护作用。     

The Protective Effects of Dexmedetomidine Preconditioning on Hepatic Ischemia/Reperfusion Injury in Rats

BackgroundIschemia/reperfusion (IR) injury is 1 of the major problems in liver surgery. This study aims to evaluate the histologic and biochemical effects of dexmedetomidine on ischemia/reperfusion injury in the liver of rats.MethodsTwenty-two Sprague-Dawley male rats were separated into 3 groups: group sham, IR (IR injury), and IR-D (IR with dexmedetomidine). Ischemia was induced for 45 minutes with portal clampage and the reperfusion period was 120 minutes. Group IR-D received 3 μg/kg of dexmedetomidine with loading for 10 minutes and then 3 μg/kg/h of dexmedetomidine was continuously injected intravenously 30 minutes before portal clampage. Biochemical factors (alanine aminotransferase and aspartate aminotransferase), variable cytokines (B cell lymphoma-2 (Bcl-2), Bax, caspase 3, caspase 8, nuclear factor-kappa B, interleukin (IL)-1β, IL-6, IL-10, mixed lineage kinase domain-like protein, and receptor-interacting protein kinase-3), and histologic findings were investigated.ResultsDexmedetomidine preconditioning significantly suppressed the histologic damage. In the IR-D group, the expression of IL-6 was decreased and the Bcl-2 was increased when compared with the IR group.ConclusionDexmedetomidine suppresses hepatic IR injury and the protective mechanism appears to involve the decrease of IL-6 and upregulation of Bcl-2 expression, which result in the attenuation of inflammatory response and the inhibition of apoptosis.     

新霉素对脑缺血再灌注损伤的保护作用

目的：探讨钙及磷酯酶Ｃ（ＰＬＣ）在脑缺血再灌注损伤中的作用机制及ＰＬＣ抑制剂新霉素是否通过抑制ＰＬＣ活性而起脑保护作用。方法：和放血降压法建立大鼠全脑缺血模型，采用原子吸收光谱法及干湿法测定缺血再灌注后脑组织含钙量。含水量变化及新霉素对其影响。结果：再灌组含钙量、含水量较对照组升高（Ｐ〈０．０５）；再灌组内随灌注时间延长，脑组织含钙量、含水量增高（Ｐ〈０．０５）；给药组含钙量、含水量均较再灌组降低     

Ischemic Preconditioning (IP) of the Liver as a Safe and Protective Technique against Ischemia/Reperfusion Injury (IRI)

The aim of the study was to evaluate safety and efficacy of IP in LT, particularly in marginal grafts. From 2007 to 2008, 75 LT donors were randomized to receive IP (IP+) or not (IP–). Considering the graft quality, we divided the main groups in two subgroups (marg+/marg–). IP was performed by 10-min inflow occlusion (Pringle maneuver utilizing a toruniquet). Donor variables considered were gender, age, AST/ALT, ischemia time and steatosis. Recipient variables were gender, age, indication to LT and MELD/CHILD/UNOS score. AST/ALT levels, INR, bilirubin, lactic acid, bile output on postoperative days 1, 3 and 7 were evaluated. Histological analysis was performed evaluating necrosis/steatosis, hepatocyte swelling, PMN infiltration and councilman bodies. Thirty patients received IP+ liver. No differences were seen between groups considering recipient and donor variables. Liver function and AST/ALT levels showed no significant differences between the main two groups. Marginal IP+ showed lower AST levels on day1 compared with untreated marginal livers (936.35 vs. 1268.23; p = 0.026). IP+ livers showed a significant reduction of moderate-severe hepatocyte swelling (33.3% vs. 65.9%; p = 0.043). IP+ patients had a significant reduction of positive early microbiological investigations (36.7% vs. 57.1%; p = 0.042). In our experience IP was safe also in marginal donors, showing a protective role against IRI.     

Protective Effect of MESNA (2-Mercaptoethane Sulfonate) Against Hepatic Ischemia/Reperfusion Injury in Rats

Purpose Reoxygenation of ischemic tissue generates various reactive oxygen metabolites (ROMs), which have a deleterious effect on various cellular functions. We evaluated the possible protective effect of 2-mercaptoethane sulfonate (MESNA) on hepatic ischemia/reperfusion (I/R) injury.Methods Wistar albino rats were subjected to 45-min hepatic ischemia, followed by 60-min reperfusion. 2-Mercaptoethane sulfonate, 150 mg/kg, or saline was given intraperitoneally (i.p.) twice, 15 min before ischemia and immediately before reperfusioin. We measured serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels to assess liver function. Liver tissue samples were taken to measure the levels of malondialdehyde (MDA), an end-product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase (MPO) activity, as an indirect index of neutrophil infiltration. We also measured hepatic collagen content, as a fibrosis marker.Results Plasma ALT and AST levels were higher in the I/R group than in the control group, but this increase was significantly decreased by MESNA treatment. Hepatic GSH levels, which were significantly depressed by I/R, increased back to the control levels in the MESNA-treated I/R group. Increases in tissue MDA levels and MPO activity caused by I/R injury decreased back to the control levels after MESNA treatment. Similarly, the increased hepatic collagen content in the I/R group decreased to the level of the control group after MESNA treatment.Conclusion The fact that MESNA alleviated I/R-induced injury of the liver and improved hepatic structure and function suggests that its antioxidant and oxidant scavenging properties may be of therapeutic value in protecting the liver against oxidative injury caused by I/R.     

细胞外高钾对离体鼠心缺血再灌注损伤的保护作用

为了解高钾抗心肌缺血再灌注（Ｉ－Ｒ）损伤的途径。用离体大鼠心脏行冠脉结扎，松扎后作电镜观察和磷酸盐－焦锑酸盐（ＰＰＡ法）细胞化学钙定位及抗氧自由基检测。结果：１３ｍｍｏｌ／Ｌ高钾保护Ｉ－Ｒ心肌超氧化物歧化酶（ＳＯＤ）活力，抑制丙二醛（ＭＤＡ）生成，减少心肌酶的漏出，保存肌膜结合钙的能力，防止钙在线粒体的积聚，减轻心肌超微结构的破坏。实验提示１３ｍｍｏｌ／Ｌ钾能抑制胞内钙超负荷和膜脂质过氧化达到抗Ｉ