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     

缺血预处理对大鼠移植肝脏保存再灌注损伤的保护及机制探讨

目的探讨缺血预处理 (ischemicpreconditioning ,IP)对大鼠移植肝脏保存再灌注损伤的保护作用及机理。方法采用SD大鼠原位肝移植动物模型 ,12 8只大鼠随机分成A(对照组 )、B(IP组 )、C(腺苷 ,Ado组 )、D(NO合成抑制剂 ,NAME组 )组 ,每组 32只。其中各组的半数用于观察存活率 ,另一半用于移植肝脏再灌注 2h后取血及肝脏检测。结果IP组和Ado组的 1周存活率、血清NO水平及肝组织腺苷含量分别为 88% (7/ 8)和 88% (7/ 8) ,(33 0± 6 1) μmol/l和 (2 9 1± 6 5 ) μmol/l,(7 2± 1 8) μmol/g和 (5 7± 1 3) μmol/g ,均高于对照组的 38% (3/ 8) ,(15 4± 3 0 )mol/L和 (3 6 9±0 5 4 ) μmol/g (P <0 0 5 ) ,血清ALT及TNF含量分别为 (2 87± 82 )IU/L和 (35 7± 93)IU/L ,(1 15± 0 2 3)ng/ml和 (1 14± 0 2 7)ng/ml,均低于对照组的 (5 88± 5 8)IU/L及 (1 5 9± 0 35 )ng/ml(P <0 0 5 ) ,组织的病理学改变也轻于对照组 ;NAME组的 1周存活率、血清NO及ALT含量等分别为 2 5 % (2 / 8)、(13 74± 3 11) μmol/l及 (6 34± 6 5 )IU/L ,与对照组相近 (P >0 0 5 ) ,而肝组织腺苷含量为 (5 5 6± 1 19)μmol/g ,与对照组差异有显著意义 (P <0 0 5 )。 结论IP对大鼠移植肝脏的保存再灌注损伤具有保护     

丹参对大鼠肝脏低温保存损伤的保护作用

目的　研究丹参对大鼠肝脏低温保存损伤的保护作用。方法　采用大鼠肝脏离体非循环灌注模型 ,观察乳酸林格液 (LR液 )中加入不同剂量丹参后保存大鼠肝脏 1 2h的效果。结果　丹参组 ( 60 0mg/g)肝组织ATP含量 ( 6.0 8± 0 .67) μmol/g及分泌胆汁量 ( 1 0 5.6± 1 2 .4) μl/h明显高于对照组 ( 2 .52± 0 .31 ) μmol/g及 ( 57.4± 8.2 ) μl/h(P <0 .0 5) ,丹参组 ( 60 0mg/g)肝组织 2 ,3 二羟苯甲酸 ( 2 ,3 DHBA) ( 0 .1 54± 0 .0 1 3)nmol/g、2 ,5 DHBA( 1 .354± 0 .0 68)nmol/g及流出液天门冬氨酸转氨酶 (AST) ( 38.4± 3.7)U/L明显低于对照组 ( 0 .2 4 5± 0 .0 2 1 )nmol/g、( 2 .1 0 5± 0 .0 97)nmol/g及( 76.4± 9.2 )U/L ,差异有显著性 (P <0 .0 5)。结论　丹参可明显提高供体肝脏的保存效果 ,其作用机理可能主要与改善低温保存肝脏的能量代谢及抗氧自由基的作用有关     

腺苷预处理对心脏直视手术心肌保护作用的临床研究

目的　探讨腺苷预处理对心脏直视手术的心肌保护效果。方法　将 30例择期心脏瓣膜置换术患者随机分成治疗组和对照组 ,治疗组在开心术前实施腺苷预处理。观察血清心肌肌钙蛋白T(cTnT)、磷酸肌酸激酶同工酶 (CK MB)、血浆丙二醛 (MDA)、心肌三磷酸腺苷 (ATP)、能量储备(EC)及心肌超微结构 (线粒体计分 )的变化。结果　主动脉开放后 30min ,治疗组cTnT为 ( 0 .42±0 .1 8) μg/L、CK MB为 ( 35.42± 1 5.87)U/L、MDA为 ( 4 .2 8± 0 .35)mmol/L升高值均明显低于对照组 [( 1 .1 6± 0 .32 ) μg/L、( 56.2 6± 1 6.36)U//L、( 6.37± 2 .46)nmol/L(P <0 .0 5) ];治疗组ATP含量( 1 5.86± 3.51 ) μmol/g干重和EC值 0 .4857± 0 .0 578均明显高于对照组 [( 6.2 5± 2 .79) μmol/g干重、0 .2 992± 0 .0 4 1 9(P <0 .0 1 ) ];治疗组线粒体计分 0 .860 2± 0 .2 381明显低于对照组 2 .740 6±0 .9792 ,(P <0 .0 1 )。结论　腺苷预处理对心脏具有明显的保护作用     

缺血预处理对大鼠减体积肝移植后Ref-1蛋白表达的影响

目的观察缺血预处理(ischemia preconditioning,IPC)对大鼠减体积肝移植术后氧化还原因子-1(redox factor-1,Ref-1)蛋白表达的影响,以探讨IPC对减体积肝移植损伤的保护作用及其机制。方法将100只Lewis成年雄性大鼠随机分成三组:IPC移植组(IPC组)、50%减体积肝移植组(PLT组)和假手术组(SO组),分别于移植后0．5 h、2 h、6 h和24 h取材,通过Western blot法和免疫组织化学技术结合图像分析定量检测移植后各时间点Ref-1表达变化,同时结合血清学和组织病理学分析Ref-1表达变化的意义。结果术后PLT组各时间点血清ALT值分别为(595．06±108．78)U/L;(723．18±117．24)U/L;(1186．65±142．31)U/L;(1498．91±126．79)U/L;IPC组术后各时间点血清ALT值分别为(459．06±84．73)U/L;(587．71±95．23)U/L;(799．61±125．97)U/L; (659．27±135．68)U/L。与PLT组相比,IPC组术后6 h和24 h血清ALT值明显降低(t=4．553, P＜0．05;t=10．110,P＜0．01)。病理学分析显示,PLT组术后24 h门静脉周围大量炎细胞浸润,肝窦扩张明显,肝组织损伤较重;而IPC组则损伤较轻。与PLT组相比,IPC组于减体积肝移植术后24 h肝实质细胞中Ref-1蛋白表达明显增高。结论缺血预处理可以减轻减体积肝移植后早期肝脏损伤,促进肝组织Ref-1蛋白表达,提示缺血预处理保护减体积肝移植物早期损伤的机制可能与促进Ref-1蛋白的表达有关。     

缺血预处理对肺缺血再灌注损伤中细胞因子生成的影响

目的　探讨缺血预处理 (IPC)对肺缺血再灌注 (I/R)损伤的保护作用及其对细胞因子生成的影响。　方法　 36只大白兔分为 3组 :对照组、I/R组和IPC组。通过阻断左肺门造成兔在体I/R损伤 ,观察IPC对肺I/R损伤的保护作用 ,指标为肺组织湿干重比、肺通透性指数及支气管肺泡灌洗液(BALF)中白细胞分类计数 ;以双抗体夹心酶联免疫吸附试验法检测血清中肿瘤坏死因子α(TNFα)、白细胞介素 6(IL 6)、白细胞介素 8(IL 8)的含量。　结果　肺I/R损伤后 ,I/R组肺组织湿干重比、肺通透性指数及BALF中性粒细胞百分比分别为 9 73± 1 1 4、(41 62± 5 77)× 1 0 - 4和 (58 1± 1 0 0 ) % ;IPC组分别为 6 2 3± 0 69、(2 0 31± 4 0 3)× 1 0 - 4和 (2 3 8± 5 2 ) % ,两组差异有极显著意义 (P <0 0 1 )。I/R组血清TNFα、IL 6和IL 8含量分别为 (0 90 78± 0 1 0 6 2 )、(0 2 1 3 7± 0 0 598)和 (0 72 1 1± 0 0 979)ng/ml,IPC组分别为 (0 7478± 0 0 843)、(0 1 2 71± 0 0 0 89)和 (0 590 3± 0 0 746)ng/ml,较I/R组显著降低 (P <0 0 1 )。　结论　IPC对I/R损伤有显著的保护作用 ,机理可能与其抑制炎性细胞因子TNFα、IL 6和IL 8的合成和释放 ,从而减轻中性粒细胞的浸润与激活有关。     

腺苷与单磷酯A联合预处理对供心保存的实验研究

目的　探讨腺苷与单磷酯A联合预处理对供心保存的效果。方法　健康大白兔 39只 ,随机分为 4组。A、B组以单磷酯A预处理 2 4h后 ,制成离体心脏 ,A组再用腺苷预处理 ;C组用腺苷作经典预处理 ;D组仅注射生理盐水作对照。各组预处理后 ,用 4℃改良St.Thomas液诱导心脏停搏 ,低温保存 4h ,复灌 1h。观察心功能恢复率、心肌三磷酸腺苷 (ATP)和丙二醛 (MDA)含量、心肌磷酸肌酸激酶 (CK mb)释放量等。结果　A、B、C、D组心功能恢复率 (+dp/dtmax ,% )分别为 :70 .97± 17.92 ,6 5 .5 4± 2 2 .6 2 ,6 4 .36± 16 .10 ,39.0 7± 13.78;A组高于B、C、D组 ,并与D组的差异有显著性 (P <0 .0 1)。A、B、C、D组心肌组织ATP含量 (10 -3 μmol/g湿重 )分别为 :5 .4 6± 1.37,3.97± 1.0 4 ,4 .4 5± 1.2 9,2 .0 7± 0 .74 ;A组高于B、C、D组 ,差异有显著性 (P <0 .0 5orP <0 .0 1)。结论　用单磷酯A和腺苷联合预处理 ,对供心有一定的保护效果。     

不同预处理中线粒体KATP通道开放对未成熟心肌的作用

目的　了解线粒体ATP敏感性钾通道 (mKATP)开放在不同预处理过程中对幼兔心脏的影响 ,并探讨其机制。方法　幼兔 (小于 2 8d) 34只随机分成 5组 ,对照组 (n =8) :平衡 30min后缺血再灌注 ;二氮嗪预处理组 (n =8) :缺血前二氮嗪 ( 10 0 μmol/L)灌注 5min后重碳酸盐缓冲液 (KH液 )冲洗 10min ,St.ThomasⅡ (STH)停跳 ;二氮嗪 + 5 羟葵酸 ( 5 HD)预处理组 (n =5 ) :二氮嗪 ( 10 0 μmol/L)和 5 HD( 10 0 μmol/L)一起灌注 5min ;缺血预处理 (IPC)组 ( n =8) :平衡 15min后全心缺血 5min ,复灌 10min行IPC ,STH停跳 ;IPC + 5 HD组 (n =5 ) :IPC前用 5 HD ( 10 0μmol/L)灌注 5min。采用LangendOrff模型 ,常温 ( 38℃ )缺血 30min ,复灌 45min。 结果　缺血 /再灌注 (I/R)后二氮嗪组的线粒体评分较IPC组 (P <0 .0 5 )和对照组 (P <0 .0 1)低 ,IPC前给予 5 HD后线粒体评分仍较对照组低 (P <0 .0 5 )。二氮嗪组和IPC组左室发展压力 (LVDP)、左室压力上升和下降最大速率 (±dp/dtmax)恢复在多个时间点上均优于对照组 ,心肌组织ATP含量高于对照组 (P <0 .0 1) ,心肌酶较对照组降低 (P <0 .0 1)。结论　二氮嗪预处理能产生与IPC相似的心肌保护作用 ,并且对线粒体的保护效果较IPC好。mKATP通道和细胞膜KATP     

缺血或药物预处理对大鼠供肝缺血再灌注损伤的抑制作用

目的　探讨缺血预处理 (IPC)或阿霉素预处理 (DPC ,模拟IPC)对大鼠供肝延迟性保护作用的发生机制。方法　将供鼠分为 3组。IPC组 :供鼠采用肝脏预先缺血 10min后再开放 ;DPC组 :供鼠经静脉注射阿霉素 (1mg/kg体重 ) ;对照组 :供鼠用等量生理盐水注射。观察各组预处理后血红素氧化酶 1(HO 1)和热休克蛋白 70 (HSP70 )含量 ;建立上述各组大鼠原位肝移植模型 ,并设假手术对照组 ,观察肝移植后各组对供肝缺血再灌注损伤的影响。结果　IPC组HO 1、HSP70含量分别于预处理 12h和 2 4h达到高峰 ;IPC和DPC组预处理 2 4h ,诱导的HSP70、HO 1含量差异无显著性 (P >0 .0 5 )。对照组肝移植后 6h ,肝组织中ICAM 1mRNA表达和内皮细胞ICAM 1分子表达明显增强 ,髓过氧化物酶 (MPO)活性增高 ,血清中天冬氨酸转氨酶 (AST)、丙氨酸转氨酶 (ALT)、乳酸脱氢酶 (LDH)及肝组织湿重 /干重 (W/D)水平明显升高 ,和假手术组相比 ,差异有显著性 (P <0 .0 1)。IPC或DPC组肝移植后减弱了ICAM 1mRNA和蛋白表达及MPO活性 ,AST、ALT、LDH及W/D的水平亦明显降低 ,与对照组比较 ,差异有显著性 (P <0 .0 5 )。结论　IPC的延迟保护作用是通过降低中性粒细胞的粘附浸润来实现的 ,这与IPC诱导生成HSP70和HO 1有关。DPC可以模拟IPC的延迟性保护     

乙醇预处理与HSP70的诱导及对肝脏缺血再灌流损伤的影响

目的探讨乙醇预处理对肝脏缺血再灌流损伤的影响以及与热休克蛋白70诱导的关系。方法雄性成年Wistar大鼠232只,胃饲乙醇浓度40%,剂量为5 g/kg体重,随机分为5组:正常对照组(N组)、胃饲乙醇组(E组)、缺血组(IR组)、生理盐水预处理组(NPC组)、胃饲乙醇预处理组(EPC组)。动物手术采用门静脉转流下的肝脏缺血模式,肝门阻断时限为90 min,于再灌流0、13、、6、12、24、72 h活杀留取血液及肝脏标本。结果EPC组3、6 h血清ALT(1 230.88±132.50、888.88±126.67)IU/L、AST(1 866.38±61.77)(、1 433.88±42.74)IU/L均明显低于IR组及NPC组,肝脏病理改变较轻,而肝组织HSP70含量高于后者。结论乙醇预处理可以减轻大鼠肝脏90 min的缺血再灌流损伤,其肝脏保护作用与肝组织HSP70升高相一致,HSP70可能是其发挥肝脏保护的物质基础之一。     

药物预处理和缺血预处理对供肝保护作用的比较研究

目的 寻找有效的砬轻供肝缺血再灌注损伤的途径。方法 建立大鼠肝脏原位隔离冷灌注模型模拟整个肝移植过程,对供肝分别作药物预处理和缺血预处理,比较正常肝,预处理供肝,末预处理供肝的ＰＣＮＡ,ＡＳＴ,ＡＬＴ,ＬＤＨ值。结果 与正常肝相比,药物预处理供肝、缺血预处理供肝、未预处理供肝肝损害程度依次加重。结论 预处理确实对供肝缺血再灌注损伤有保护作用;药物预处理的效果可能优于缺血预处理。     

缺血预适应的研究进展

1986年Murry等[1]首次提出:心肌在经受了一次或多次短暂的缺血再灌注后对随后更长时间致死性缺血再灌注损伤的耐受性增强.并将此现象命名为缺血预适应(Ischemic preconditioning IPC).经过15年大量的动物实验及临床试验,对IPC的特点、触发因素、发生机理及结果进行了深入的研究,使人们对缺血再灌注损伤及IPC有了深一步的认识.     

Ischemic versus pharmacologic hepatic preconditioning

Background

Hepatic ischemia–reperfusion injury has a significant impact on liver resection and transplantation. Many strategies have been developed to reduce the effects of ischemia–reperfusion injury, including pharmacologic and ischemic preconditioning; however, studies comparing these two methods are lacking.

Material and methods

An experimental study was performed in a swine model. Eighteen swine were randomly assigned to three different groups: an ischemic preconditioning (IschPC) group, a pharmacologic preconditioning (PharmPC) group, and a control group. All animals underwent a 40-min liver ischemia, followed by 40 min of reperfusion. The IschPC group received a short period of ischemia (10 min) and a short period of reperfusion (15 min) before prolonged ischemia. The PharmPC group received inhaled sevoflurane for 30 min before prolonged ischemia. The control group did not receive any intervention before prolonged ischemia. Blood samples and liver tissue were obtained after ischemic and reperfusion periods. Injury was evaluated by measure of DNA damage (using COMET assay) and serum biochemical markers (transaminases, alkaline phosphatase, amylase, bilirubin, and C-reactive protein [CRP]).

Results

No significant difference was found in serum biochemical markers, except for the C-reactive protein level that was lower in the PharmPC group than in the control group soon after hepatic ischemia. Soon after prolonged ischemia, DNA damage index, both in blood samples and in liver tissue samples, was similar among the groups. However, an increase in DNA damage after reperfusion was higher in the control group than in the PharmPC group (P < 0.05). The increase in DNA damage in the IschPC group was half of that observed in the control, but this difference was not statistically significant.

Conclusions

Our results suggest an early protective effect of PharmPC (lower levels of C-reactive protein soon after ischemia). The protective effect observed after reperfusion was higher with PharmPC than with ischemic preconditioning. The simultaneous use of both methods could potentiate protection for ischemia–reperfusion.     

TNF-alpha is required for late ischemic preconditioning but not for remote preconditioning of trauma

BACKGROUND: Ischemic preconditioning (IPC) and remote IPC are cardioprotective phenomena in which ischemia of the myocardium or of a remote tissue, respectively, induces cardioprotection. Despite clinical evidence that surgical trauma can remotely affect myocardial infarction, to date there are no basic science studies addressing the effect of nonischemic trauma at distant sites upon cardiac ischemia/reperfusion (I/R) injury. The objectives of this study were to determine the effects of nonischemic remote surgical trauma upon infarct size after myocardial I/R and to determine the effects of TNF-alpha ablation upon cardioprotective phenomena. MATERIALS AND METHODS: A minimally traumatic mouse model was used to ascertain the effect of remote nonischemic surgical trauma upon I/R injury. TNF-alpha knockout mice were employed to determine the effect of TNF-alpha ablation. RESULTS: Carotid artery vascular surgery remotely exacerbates cardiac I/R injury increasing infarct size by 287% (remote cardiac injury or RCI). Nonischemic, nonvascular trauma (abdominal incision) results in remote preconditioning of trauma (RPCT), decreasing infarct size by 81% (early phase) and 40% (late phase) relative to controls. Finally, TNF-alpha is required for late IPC but is not necessary for RCI or for RPCT. CONCLUSIONS: We show that late IPC is TNF-alpha-dependent and describe two unique TNF-alpha-independent remote effects of nonischemic trauma upon myocardial infarction. Understanding the mechanism of these remote effects will allow the development of novel therapies for the treatment of ischemic heart disease. RPCT and TNF-alpha ablation have an additive protective effect suggesting that combinations of complementary approaches may be a useful strategy for maximizing the clinical efficacy of cardioprotective therapies.     

Ischaemic preconditioning of the brain,mechanisms and applications

Summary Background. The concept of ischaemic preconditioning was introduced in the late 1980s. The concept emerged that a brief subcritical ischaemic challenge could mobilize intrinsic protective mechanisms that increased tolerance against subsequent critical ischaemia. Tissues with a high sensitivity against ischaemia, i.e. myocardium and central nervous system, present the most promising targets for therapeutic application of ischaemic preconditioning. During the last years the mechanisms of neuronal preconditioning were systematically studied and a number of molecular regulation pathways were discovered to participate in preconditioning. The purpose of the present review is to survey the actual knowledge on cerebral preconditioning, and to define the practical impact for neurosurgery. Methods. A systematic medline search for the terms preconditioning and postconditioning was filed. Publications related to the nervous system were selected and analysed. Findings. Preconditioning can be subdivided into early and late mechanisms, depending on whether the effect appears immediately after the nonlethal stress or with a delay of some hours or days. In general early effects can be linked to adaptation of membrane receptors whereas late effects are the result of gene up- or downregulation. Not only subcritical ischaemia can trigger preconditioning but also hypoxia, hyperthermia, isoflurane and other chemical substances. Although a vast amount of knowledge has been accumulated regarding neural preconditioning, it is unknown whether the effects can be potentiated by pharmacological or hypothermic neuroprotection during the critical ischaemia. Furthermore, although the practical importance of these findings is obvious, the resulting protective manipulations have so far not been transferred into clinical neurosurgery. Postconditioning and remote ischaemic preconditioning are additional emerging concepts. Postconditioning with a series of mechanical interruptions of reperfusion can apparently reduce ischaemic damage. Remote ischaemic preconditioning refers to the concept that transient ischaemia for example of a limb can lead to protection of the myocardium and possibly the brain. Conclusion. Possible cumulative neuroprotection by preconditioning and pharmacological protection during critical ischaemia should be studied systematically. Easy to apply methods of preconditioning, such as the application of volatile anaesthetics or erythropoietin some hours or days prior to planned temporary ischaemia, should be introduced into the practice of operative neurosurgery.     

吸入麻醉药预处理的心肌保护机制

吸入麻醉药对心肌具有预处理作用,这为围手术期心肌保护的研究和应用提供了新方法.目前有关吸入麻醉药预处理的机制尚未完全阐明,此文综述了吸入麻醉药在活性氧产生、细胞内信号转导、ATP敏感性钾通道开放及细胞凋亡通路调节等方面的研究进展.     

吸入麻醉药心肌预处理的信号转导机制

吸入麻醉药预处理有IPC样的心肌保护作用,其作用机制目前尚未完全阐明。吸入麻醉药预处理的信号转导机制可能与IPC的信号转导途径相似,吸入麻醉药可能刺激心肌产生触发因子,然后启动级联反应,激活效应因子,发挥预处理效应。目前为止,研究已证实ROS、G蛋白耦联受体、蛋白激酶、线粒体和肌膜KATP通道（Mito KATP and Sarc KATP）介导APC。现就吸入麻醉药心肌预处理信号转导机制方面的最新进展作一综述。     

腺苷预处理保存供心的实验研究

目的　本研究探讨腺苷预处理早发效应对供心的保护效果。方法　大白兔制成离体心脏 ,以腺苷预处理后 4℃改良St .Thomas液诱导心脏停搏 ,置于该液中低温保存 4h ,再灌注 1h。观察心功能恢复率、心肌ATP、Ck -mb释放量。另设缺血预处理组和单纯改良St .Thomas液保存对照组。结果　缺血和腺苷预处理心功能恢复率 ( +dp/dtmax % )分别为 ( 74.5 6± 14 .3 8) ,( 68.3 8± 10 .47) ,均高于对照组 ( 3 2 .45± 9.46) ,差异有显著性 (P <0 .0 5 )。结论　腺苷预处理早发效应能改善供心保存效果。     

Normobaric hyperoxia preconditioning ameliorates cisplatin nephrotoxicity

Background: Cisplatin is a potent anticancer drug, but its nephrotoxicity limits the clinical use of it. To reduce the Cisplatin-induced nephrotoxicity, various interventions have been implicated. The aim of this study was to examine whether preconditioning with normobaric hyperoxia would prevent Cisplatin-induced nephrotoxicity in patient with solid tumor. Methods: In a prospective study, 80 adult patients with solid tumor who were treated with Cisplatin between February 2011 and December 2011 were included. Forty-three patients were exposed to pure oxygen via non-rebreathing reservoir mask which increased the provided oxygen rate to 60% oxygen for 2 hours at 48, 24, and 6 hours before intravenous administration of Cisplatin and 37 patients received only Cisplatin as a control group. Estimated glomerular filtration rate (eGFR) calculated in all patients on day 1 before and on days 1, 3, 6, 30 after Cisplatin exposures. Results: Patients treated with Cisplatin and 60% oxygen showed a mild improvement in eGFR and mild reduction of serum creatinine after 30 days with statistically mild significant differences (p?=?0.048). Conclusion: This study showed that normobaric and intermittent precondition of 60% oxygen prior to Cisplatin treatment had an acute transient adverse effect on renal function; however, the improvement of renal function will be seen after 30 days. Thus, it may help to prevent Cisplatin nephrotoxicity.     

肢体缺血预适应的远程脏器保护作用

肢体和内脏等严重的缺血再灌注（IR）损伤可引起全身炎性反应（SIRS）并伤及远隔器官,但短时间IR却有缺血预适应（ischemia preconditioning,IPC）作用,能提高脏器的缺氧耐受。近年来动物实验中不同脏器间的远程预适应现象（remote preconditioning,RPC）日益受到关注,如肠缺血的心肌保护、肝缺血的肾保护作用等。