Ischemic Preconditioning Protects the Pig Liver by Preserving the Mitochondrial Structure and Downregulating Caspase-3 Activity

Summary Background Data: The beneficial effects of ischemic preconditioning (IPC) on hepatic ischemia-reperfusion injury (I/RI) have been described. However, the way in which IPC causes the changes in mitochondrial ultrastructure seen in hepatic I/RI is not well understood. Objective: The objective of the present study was to determine whether IPC protects the liver from changes in mitochondrial structure and caspase 3 activity in the early phase of post-ischemic injury. Methods: A pig model consisting of 90 min of hepatic ischemia and 180 min of reperfusion was employed. Eighteen female pigs were randomly divided into three groups: sham-operated, non-preconditioned, and ischemic preconditioned (10 min ischemia followed by 10 min reperfusion). Serum concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and thiobarbituric acid reactive substances (TBARS), as well as bile flow, were measured. Liver biopsies were taken after reperfusion for histological, immunohistochemical (anti-caspase 3), and ultrastructural examinations. Results: The IPC procedure increased bile flow (p < 0.01), reduced serum AST level (p < 0.01), and reduced serum concentration of TBARS at 180 min of reperfusion (p = 0.05). Ischemic-preconditioned liver cells had less caspase 3 activity than the non-preconditioning group (p < 0.01), and changes in mitochondrial ultrastructure were reduced (p < 0.01). Conclusion: IPC exerts a powerful protective effect against hepatic I/RI in the early phase of reperfusion, which may be mediated by preservation of mitochondrial structure and inhibition of caspase-3 activity.     

缺血预适应对老年大鼠缺血-再灌注心肌的影响

目的探讨缺血预适应（ischemic preconditioning,IPC）对老年大鼠缺血-再灌注损伤（I/R）后心肌的影响。方法取Wistar大鼠56只,其中21~23月龄（老年鼠）和4~5月龄（青年鼠）各28只,建立离体心脏Langendorff灌注模型,按随机数字表法分为7组（每组8只）：青年对照组、青年I/R组、青年IPC组、老年对照组、老年I/R组、老年IPC组、老年强化IPC组。对照组采用全心灌流90 min,不做任何处理;I/R组采用心脏平衡灌流30min后,缺血30 min,再复灌30     

肾缺血预处理对肾小管上皮细胞内钙超载的影响

目的：通过观察肾缺血预处理（IPC）和缺血再灌注（I/R）过程中血清超氧化物歧化酶（SOD）、丙二醛（MDA）和细胞内游离钙离子浓度（[Ca^2＋]i）含量的变化,进一步探讨肾IPC的保护机制。方法：将雄性SD大鼠88只随机分为11组,摘除右肾,分离并夹闭左肾动脉制备肾I/R和缺血预处理后缺血再灌注（IPC-I/R）动物模型。Ⅰa～Ⅴa（I/R）组为缺血再灌注0、1、24、48、72h组,Ⅰb～Ⅴb（IPC-I/R）组为缺血预处理后缺血再灌注0、1、24、48、72h组,Sham组为假手术组。比色法测定血清肌酐（Scr）、尿素氮（BUN）、SOD、MDA含量,流式细胞仪检测肾小管上皮细胞内[Ca^2＋]i水平,TUNEL原位标记法观察细胞凋亡情况。结果：除0h组外,IPC-I/R与I/R各组比较肾功能损害、细胞凋亡均明显减轻,SOD升高,MDA降低,[Ca^2＋]i水平下降;两种模型中均以再灌注24h组损伤最严重,Scr、BUN、MDA和[Ca^2＋]i水平最高,SOD水平最低,细胞凋亡最多;再灌注24h前损伤呈加重趋势,24h后逐渐减轻;组间比较,[Ca^2＋]i与血清SOD水平呈负相关,与MDA呈正相关。结论：肾IPC可以减轻I/R过程中膜脂质过氧化损伤和细胞内钙超载,从而减轻肾脏形态及功能损伤;膜脂质过氧化和细胞内钙超载相互作用,共同发挥对肾I/R损伤的保护作用。     

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     

过氧化物酶体增殖物激活受体γ协同刺激因子1α在早期缺血预处理中的作用

目的探讨过氧化物酶体增殖物激活受体γ协同刺激因子1α（PGC-1α）在早期缺血预处理中的作用和早期缺血预处理的机制。方法取Wistar大鼠30只,建立离体心脏Langendorff灌注模型,随机分成3组,每组10只。对照组（CON组）：全心灌流120min,不做任何处理;缺血-再灌注组（I/R组）：心脏平衡灌流30min后,缺血30min,再灌注60min;缺血预处理组（IPC组）：心脏平衡灌流10min,经2次缺血5min复灌5min后,缺血30min,再灌注60min。采用链霉素抗生物素蛋白-过氧化物酶（S-P法）检测PGC-1α的表达,测定平均积分光密度值（IODA）;采用电子显微镜对心肌线粒体进行Flameng评分。结果IPC组PGC-1α表达（IODA10.94±5.23）明显高于I/R组（IODA3.88±1.72）和CON组（IODA3.39±2.46;P=0.009,0.007）。I/R组线粒体水肿、破裂明显,而CON组、IPC组线粒体损伤较轻。Flameng评分分析显示,IPC组（0.44±0.13）和CON组（0.88±0.22）线粒体评分低于I/R组（1.78±0.14;P=0.003,0.014）。结论IPC能明显减轻线粒体损伤,其机制与PGC-1α激活和高度表达有关,PGC-1α可能是一种重要的内源性心肌保护物质。     

MicroRNA-1和microRNA-21在缺血预处理、后处理及远端预处理中的表达变化

目的 通过离体缺血-再灌注心脏模型,观察缺血预处理(IPC)、缺血后处理(IPO)和肢体远端预处理(RIPC)后心脏microRNA1(miRNA-1)和microRNA21 (miRNA-21)的表达变化,以及它们所调控靶蛋白热休克蛋白70 (HSP70)和程序性细胞死亡4(PDCD4)表达变化,期望从miRNA调控水平揭示心脏的内源性保护机制.方法 取Sprague-Dawley (SD)大鼠心脏,建立离体Langendorff心肌缺血-再灌注模型,随机分为4组(每组12只),对照组、IPC组、IPO组和RIPC组.检测各组血流动力学指标,蛋白印迹法(Western blotting)检测PpDCD4、HSP70、B细胞淋巴瘤/白血病-2(Bc1-2)和Bc1-2相关X蛋白(Bax)含量,taqman探针法检测miRNA-1和miRNA-21含量,末端脱氧核苷酸转移酶介导的原位缺口标记法(TUNEL)检测心肌细胞凋亡,2,3,5-氯化三苯基四氮唑(TTC)法检测心肌梗死面积. 结果 IPC组心肌的miRNA-1和miRNA-21表达明显高于对照组,但RIPC组和IPO组心肌的miRNA-1表达较对照组明显降低( P＜0.05).IPC组、RIPC组和IPO组心肌中HSP70、PDCD4和Bax蛋白含量较对照组明显减少(P＜ 0.05),Bc1-2蛋白含量各组间差异无统计学意义.IPC组、RIPC组和IPO组左室心肌梗死面积/左室总面积以及心肌细胞凋亡率明显低于对照组(P＜ 0.05). 结论 miRNA-1和miRNA-21在缺血预处理、缺血后处理和远端预处理后,表达变化是不同的,同时各处理组中miRNA与其靶蛋白并不都是负性调节关系.     

肾缺血/再灌注时肾组织损伤及细胞凋亡的实验研究

目的：检测肾缺血／再灌注不同时问点肾组织、功能损伤及细胞凋亡的变化，探讨细胞凋亡在肾缺血／再灌注损伤中发生的机制。方法：应用苦味酸法和二乙酰一肟反应法测定大鼠肾缺血／再灌注不同时间点血肌酐和尿素氮值检测肾功能变化，用HE染色光镜下观察缺血／再灌注石蜡包埋切片肾组织损伤形态学改变，用酚／氯仿抽提小片断DNA，在琼脂糖电泳上测定不同时间点DNA Ladder及利用原位凋亡检到法观察各时间点TUNEL阳性细胞数检测细胞凋亡情况。结果：肾功能检测发现，缺血45min后血肌酐和尿素氮值明显增高和正方对照差异显(P＜0.05)，再灌注早期上升缓慢，3h后再次增高，组内对比差异显(P＜0．05)。HE染色光镜下观察肾组织细胞以近端肾小管变性为主、坏死轻微，缺血／再灌注各时间点组织损伤变化与肾功能变化规律相一致。琼脂糖电泳和TUNEL检测在缺血45min再灌注3h时可测到DNA Ladder和TUNEL阳性细胞增加，再灌注12h细胞凋亡最明显。结论：肾缺血／再灌注可引起肾组织轻、中度的损伤和明显的肾功能损害；肾缺血／再灌注后期肾组织及功能损伤加重可能与细胞凋亡的发生有关。     

Efeitos de dexmedetomidina em conjunto com o pré‐condicionamento isquêmico remoto em lesão de isquemia‐reperfusão renal em ratos

Background and objectivesThe aim of this study was to evaluate the effects of remote ischemic preconditioning by brief ischemia of unilateral hind limb when combined with dexmedetomidine on renal ischemia–reperfusion injury by histopathology and active caspase‐3 immunoreactivity in rats.Methods28 Wistar albino male rats were divided into 4 groups. Group I (Sham, n = 7): Laparotomy and renal pedicle dissection were performed at 65th minute of anesthesia and the rats were observed under anesthesia for 130 min. Group II (ischemia–reperfusion, n = 7): At 65th minute of anesthesia bilateral renal pedicles were clamped. After 60 min ischemia 24 h of reperfusion was performed. Group III (ischemia–reperfusion + dexmedetomidine, n = 7): At the fifth minute of reperfusion (100 μg/kg intra‐peritoneal) dexmedetomidine was administered with ischemia–reperfusion group. Reperfusion lasted 24 h. Group IV (ischemia–reperfusion + remote ischemic preconditioning + dexmedetomidine, n = 7): After laparotomy, three cycles of ischemic preconditioning (10 min ischemia and 10 min reperfusion) were applied to the left hind limb and after 5 min with group III.ResultsHistopathological injury scores and active caspase‐3 immunoreactivity were significantly lower in the Sham group compared to the other groups. Histopathological injury scores in groups III and IV were significantly lower than group II (p = 0.03 and p = 0.05). Active caspase‐3 immunoreactivity was significantly lower in the group IV than group II (p = 0.01) and there was no significant difference between group II and group III (p = 0.06).ConclusionsPharmacologic conditioning with dexmedetomidine and remote ischemic preconditioning when combined with dexmedetomidine significantly decreases renal ischemia–reperfusion injury histomorphologically. Combined use of two methods prevents apoptosis via active caspase‐3.     

低温对缺血预调心肌保护作用的影响

目的:为确定体外循环心脏直视手术时应用"缺血预调"(IPC)的可能性,分别在两部分实验中研究了(1)IPC对长时间低温缺血心肌的保护作用.(2)IPC期间心肌低温对IPC诱导心肌保护作用的影响.方法:建立离体灌注的大鼠工作心脏模型,稳定后施行不同的预调方案,进而缺血停搏.在预调处理前和缺血再灌注后两次测定工作心脏的主动脉流量(AF).在第一部分研究中,离体心脏在18℃低温条件下缺血60分钟,IPC方案为1b组:5分钟缺血+5分钟再灌注(5×1);1c组:5分钟缺血+5分钟再灌注,反复2次(5×2);1d组:5分钟缺血+5分钟再灌注,反复3次(5×3).1a组为对照组,缺血前不施行预调处理.在第二部分研究中,离体心脏在37℃条件下常温缺血15分钟,实验组(包括6组:Ⅱ,Ⅲ,Ⅳ,Ⅴ,Ⅵ和Ⅶ组)的预调方案均为5×1,但IPC期的心肌温度不同,其中:Ⅱ组为37℃,Ⅲ组32℃,Ⅳ组27℃,Ⅴ组22℃,Ⅳ组17℃,Ⅶ组12℃.Ⅰ组为对照组,缺血前不施行预调处理.结果:在第一系列研究中,对照组的主动脉流量(AF)仅恢复到缺血前的2.7%.预调各组的AF恢复程度显著提高,与对照组比较1b组为22%(P＜0.01),1c组为34%(P＜0.0,1d组为14,9%(P＜0.05).5×2的预调方案具有最强的心肌保护作用.在第二系列研究中,预调期温度高于22℃的各组AF恢复程度显著提高.其中Ⅱ组为76%,Ⅲ组70%,Ⅳ组71%,Ⅴ组62%.而对照组AF恢复不足20%(Ⅱ、Ⅲ、Ⅳ、Ⅴ组与对照组比较,P＜0.05),Ⅵ组和Ⅶ组的AF恢复值与对照组比较差异均不显著,表明IPC期心肌温度低于22℃时,无心肌保护作用.结论:无论在常温或低温(＞22℃)条件下进行缺血预调均有显著的心肌保护作用,IPC有可能应用于改进体外循环合并中度低温时心脏手术的心肌保护.     

缺血预处理对大鼠移植胰腺缺血再灌注损伤的保护作用及其机制的研究

目的：探讨缺血预处理对大鼠移植胰腺冷缺血再灌注损伤和细胞凋亡的保护作用及其机制。方法：24只糖尿病SD大鼠随机分为缺血再灌注组（I/R组,n=6）和缺血预处理组（IPO组,n=18）,IPO组又根据不同方法分为3个亚组：IPO1组（再灌注30s,缺血30s1次,n=6）、IPO2组（再灌注30s,缺血30s3次,n=6）和IPO3组（再灌注30s,缺血30s6次,n=6）。24只SD大鼠为供体,I/R组和IPO组均行同种胰腺移植。另取6只SD大鼠为对照组。检测各组再灌注前、后血糖及再灌注后2h移植胰腺组织中SOD和MDA含量;TUNEL法观察移植胰腺组织细胞凋亡情况,WesternBlot检测移植胰腺组织Bax和Bcl-2蛋白表达情况。结果：1）再灌注后IPO各组相对于I/R组血糖低（P〈0.05,P〈0.01,P〈0.05）;IPO2组较IPO1组和IPO3组血糖低（P均〈0.05）;2）再灌注后IPO组较I/R组移植胰腺组织中SOD含量高（P均〈0.01）,MDA含量低（P均〈0.01）,IPO2组相对于IPO1组和IPO3组SOD含量高（P均〈0.05）、MDA含量低（P均〈0.05）。3）再灌注后IPO组较I/R组移植胰组织中AI值低（P均〈0.01）,IPO2组相对于IPO1组和IPO3组AI值低（P均〈0.05）;4）I/R组胰组织Bax蛋白高表达,Bcl-2蛋白低表达,IPO各组再灌注后移植胰组织Bax蛋白低表达,Bcl-2蛋白高表达,而IPO2组Bcl-2蛋白表达最高,Bax蛋白表达最低。结论：缺血预处理对大鼠移植胰腺的缺血再灌注损伤具有保护作用,并可以减少移植胰腺缺血再灌注后的细胞凋亡,机制与减少氧自由基、上调Bcl-2蛋白和下调Bax蛋白有关。再灌注30s缺血30s重复3次是最佳的大鼠移植胰缺血预处理诱导办法。     

缺血预处理对肺缺血-再灌注损伤的保护作用及机制

目的　探讨缺血预处理 (IP)对肺缺血 -再灌注 (IR)损伤的保护作用和可能的机制。　方法　建立兔在体IR损伤模型 ,将 36只兔随机分为 IP组、IR组和对照组 ,每组 12只 ,观察各组肺湿 /干重比 ,检测各组肺组织超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量及髓过氧化物酶 (MPO)活性 ,对支气管肺泡灌洗液 (BAL F)中白细胞进行分类计数 ,并检测各组肺通透性指数。　结果　 IP组与 IR组比较 ,肺湿 /干重比明显降低 (P<0 .0 1) ;肺组织中 SOD活性显著增高 ,MDA含量和 MPO活性明显降低 (P<0 .0 1) ;BAL F中中性粒细胞分类计数、肺通透性指数明显降低(P<0 .0 1)。IP组与对照组比较 ,上述指标差别无显著性意义 (P>0 .0 5 )。　结论　 IP可通过减轻 IR时肺组织中性粒细胞的浸润与激活 ,提高机体抗氧化自由基的能力 ,而减轻 IR引起的肺损伤。     

常温缺血预处理对幼兔未成熟心肌的保护作用

目的研究常温缺血预处理(IP)对幼兔未成熟心肌的保护作用。方法将24只幼兔分为四组。组1IP1次;组2IP2次;组3IP3次;对照组。应用Langendorff心脏灌注方法,对3～4周龄幼兔离体心脏实施不同次数的5分钟缺血、5分钟再灌注的常温IP,常温缺血45分钟,再灌注30分钟。于平衡灌注末、缺血前、再灌注3分钟、5分钟、10分钟、20分钟和30分钟分别测定左心室发展压(LVDP)、左心室最大上升及下降速率(±dp/dtmax),再灌注末测定心肌组织三磷酸腺苷(ATP)含量、丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果再灌注30分钟时,组1和组2LVDP、+dp/dtmax恢复率显著高于对照组（P<0.05,P<0.01）,组3LVDP、±dp/dtmax的恢复率与对照组比较差别无显著性意义。再灌注末组1、组2和组3心肌ATP含量显著高于对照组（P<0.05）。组2MDA含量显著低于组1、组3和对照组（P<0.05）。结论IP对未成熟心肌具有保护作用,其中2次IP的保护作用最好,而3次的保护作用减弱,表明IP对未成熟心肌的保护作用具有饱和效应和累计现象。     

缺血预处理时间对大鼠骨骼肌缺血再灌注损伤保护作用的影响

目的探讨缺血预处理时间与骨骼肌缺血再灌注损伤保护作用之间的关系. 方法 36只大鼠随机分成 6组,制成切断患肢皮肤、肌肉和神经,仅保留股动静脉的动物模型.A组:直接缺血4 h再灌注;B、C、D和E组:分别缺血5、10、15和20 min,再灌注5、10、15和20 min,重复3次后缺血4 h再灌注;F组:制成仅保留股动静脉的左大腿组织块模型,未经过缺血处理.通过测定丙二醛(malondialdehyde, MDA)、骨骼肌水肿和坏死程度,观察不同预缺血时间对骨骼肌缺血再灌注损伤的保护作用. 结果对骨骼肌缺血后再灌注,预缺血5 min对骨骼肌即有保护作用,肌肉存活面积达82.47%;预缺血10和15 min肌肉存活面积增至最高,达89.03%和89.49%;预缺血20 min肌肉存活面积降至78.27%.预缺血5 min即可减轻骨骼肌水肿;预缺血10 min骨骼肌水肿程度最轻;预缺血15 min水肿程度又加重,预缺血20 min水肿程度继续加重.预缺血5、10和15 min MDA水平均降低,预缺血20 min MDA水平与单纯缺血再灌注组相同. 结论预缺血时间对大鼠骨骼肌缺血再灌注损伤的保护作用呈现先增强后减弱的趋势,以预缺血10 min保护作用最强.     

缺血预处理在肠缺血/再灌注损伤中的研究进展

缺血预处理是近年来提出的一种新的肠缺血/再灌注损伤的保护方法,即使在小肠长时间缺血/再灌注之前,进行一次或多次短暂的缺血,再灌注过程.研究表明缺血预处理对小肠缺血/再灌注损伤具有保护作用,但机制复杂,尚未明确.现就缺血预处理在肠缺血,再灌注损伤中的研究进展作一综述.     

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.     

Modulation of Remote Ischemic Preconditioning by Proinflammatory Cytokines in Renal Transplant Recipients

Aim: Remote ischemic preconditioning (RIPC) has been used as a strategy to reduce acute renal injury and ischemia-reperfusion injury (IRI) in renal transplantation (RT) with controversial results. Objective: To determine if RIPC modifies IRI in cadaveric RT recipients through inflammatory mediators and graft function. Methods: Twenty-nine RT recipients were studied, 12 in the control group (CG) and 17 in the RIPC group. RIPC which was performed on donors using a pneumatic tourniquet placed on both thighs for 10 min followed by the determination of IL-1, IL-6, TNF-α, VEGF, and ICAM-1, and hematological and biochemical parameters in different phases of RT. Results: Serum creatinine levels were significantly lower in the RIPC group versus the CG at 15 and 30 days; however, the estimated glomerular filtration rate (eGFR) showed no significant difference in any phase between either group, only TNF-α showed significantly higher values in the RIPC group versus the CG in almost all phases of the study, meanwhile IL6 was increased at 72 hours (hr) and 30 days, IL1 at 72 hr and 15 days and ICAM-1 post reperfusion, contrary to this VEGF showed a decrease at 7 and 15 days. Conclusion: RIPC did not improve eGFR or serum creatinine; however, it modifies the inflammatory response in RT recipients.     

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。