腺苷及缺血后处理对兔缺血再灌注心肌的保护作用

目的 探讨腺苷对缺血再灌注后心肌的保护作用,及其与缺血后处理的关系.方法 40只健康大耳白兔,随机分为对照组、拮抗剂组、缺血后处理组、腺苷治疗组4组,每组10只.制备在体兔心肌缺血再灌注模型,检测心肌收缩功能指标,测量心肌梗死范围,观察缺血再灌注即刻应用腺苷及缺血后处理对兔缺血再灌注后心肌的影响.结果 腺苷治疗组和缺血后处理组与对照组和拮抗剂组相比,再灌注之后左室内压峰值、左室内压最大上升速率和左室内压最大下降速率的恢复率差异有统计学意义(P＜0.05);梗死范围均明显低于对照组和腺苷受体拮抗剂组(P<0.01);心肌酶学LDH和CK含量较对照组和腺苷受体拮抗剂组明显降低(P<0.01).结论 腺苷/腺苷受体途径是缺血后处理的重要途径之一,能够减轻缺血再灌注损伤,保护心肌.     

缺血后处理对肝脏缺血再灌注的保护机制研究进展

肝脏移植是治疗终末期肝病的唯一有效手段,缺血再灌注损伤是移植肝功能受损乃至丧失的主要因素之一.缺血后处理是在组织器官长时间缺血后再灌注早期,对组织器官进行数次短暂的再灌注/阻断的处理方法.众多研究显示,缺血后处理对肝脏缺血再灌注损伤有保护作用.他发挥作用的可能机制,主要是通过对氧自由基、钙超载、中性粒细胞、细胞因子、细胞凋亡、线粒体等几个方面的作用来实现.     

缺血后处理在心肌保护中的研究进展

缺血后处理是保护心肌的一种新方法,其机制与抑制氧自由基堆积、抑制钙超载、抑制中性粒细胞的活化及激活再灌注损伤的补救激酶途径和ATP敏感性钾通道开放等有关。     

心肌后处理保护机制的研究进展

<正>心肌梗死属冠心病的严重类型,是因冠状动脉血供急性减少或中断,使相应的心肌严重而持久地急性缺血导致的心肌坏死。早期再灌注是挽救缺血心肌的唯一方法,恢复血流灌注可防止梗死面积扩大,保护心脏功能。目前心肌梗死的再灌注治疗主要有溶栓和冠状动脉介入治疗,但再灌注开始的几分钟内,由于细胞内钙超载、三磷酸腺苷(adenosine triphosphate,ATP)合成不足、氧自由基爆发及膜磷脂的缺失而产生不可逆的细胞损害,包括心肌细胞坏死、凋亡,心肌收     

ERK参与缺血后处理的心肌保护作用机制研究

目的 观察缺血后处理对大鼠心肌缺血-再灌注损伤的保护作用,并探讨其可能的机制.方法 选择Wistar大鼠24只,建立大鼠心肌缺血-再灌注损伤模型,随机分为3组:对照组(I/R组)、缺血后处理组(I-postC组 )、抑制剂组(I-postC+ERK抑制剂组).再灌注结束后腹主动脉插管取血测定血清生化指标,剖取左心室计算心肌梗死面积.结果 与I/R组相比,I-postC组心肌梗死面积减少,血清乳酸脱氢酶(LDH)、心肌肌酸激酶同工酶(CK-MB)活性及丙二醛(MDA)含量降低,血清超氧化物歧化酶(SOD)活性增加;抑制剂组与I-postC组相比,心肌梗死面积增大,血清LDH、CK-MB活性及MDA含量升高,血清SOD活性减弱.结论 心肌缺血后处理对实验性大鼠心肌缺血-再灌注损伤有明显的保护作用,该作用可能与细胞外调节蛋白激酶(ERK)信号传导通路有关.     

缺血后处理对心肌缺血再灌注损伤的保护作用

缺血后处理是指在缺血发生后、长时间的再灌注之前,对心脏进行数次短暂的再灌注/缺血循环的处理方法.与缺血预适应一样,缺血后处理能减轻再灌注后心肌的损伤.由于缺血后处理可在心肌缺血发生后应用,所以比缺血预适应具有更大的临床应用价值.     

STEMI急诊介入治疗中缺血后处理对心肌的保护作用

目的:探讨ST段抬高型心肌梗死(STEMI)急诊介入治疗中缺血后处理对心肌的保护作用。方法:选择广西医科大学附属医院2011年1月~2012年12月心内科住院,且在12h内行冠状动脉介入治疗(PCI)的82例STEMI患者,根据处理方法不同分为缺血后处理组(42例)和单纯再灌注组(40例),评价两组心功能情况等。结果:与单纯再灌注组比较,缺血后处理组ST段完全回落率(55.0%比81.0%)、左室射血分数[(0.5±0.1)比(0.7±0.1)]明显提高,心律失常率(60.0%比21.4%),室壁运动计分[WMSI,(2.0±0.7)分比(1.3±0.6)分]、心肌梗死面积[MIS,(15.1±7.1)%比(9.9±5.3)%]、核素心肌灌注缺损范围分数[ES,(0.4±0.1)%比(0.2±0.1)%]和核素心肌灌注缺损严重程度积分[SS,(2.3±1.1)%比(1.8±1.2)%]均显著减少(P<0.05~<0.01)。结论:缺血后处理可显著改善ST段抬高型心肌梗死患者心肌缺血再灌注损伤程度,保护心肌组织。     

缺血预处理与缺血后处理对犬肾缺血再灌注损伤的作用及机制探讨

目的观察缺血预处理（IPC）与缺血后处理（IPO）对犬肾缺血再灌注损伤的作用,并探讨其机制。方法24只成年雄性杂种犬随机分为4组,各6只,均开腹、游离双肾。假手术组（S组）：切除右肾,缝合腹壁;缺血再灌注组（I／R组）：切除右肾、游离左肾后,左肾动、静脉夹闭60min后恢复灌流;缺血预处理组（IPC组）：在左肾动、静脉夹闭前先予5min的缺血、5min的再灌,共3次,然后恢复灌流：缺血后处理组（IPO组）：在肾动、静脉夹闭60min后立即再灌注30s、再缺血30s,共6次,然后恢复灌流。结果术后3d,IPC,IPO组与I／R组相比,血清肌酐（Cr）、尿素氮（BUN）浓度降低（P均〈0．05）。与I／R组相比,IPC、IPO组超氧化物歧化酶（SOD）活性升高、丙二醛（MDA）浓度降低、髓过氧化物酶（MPO）含量下降、细胞凋亡指数（M）降低（P均〈O．05）,肾脏病理损伤明显减轻。结论IPC与IPO都能减轻肾缺血再灌注损伤,其机制可能与减轻肾脂质过氧化反应及抑制细胞凋亡、减轻炎症反应有关。     

缺血后处理对高血脂大鼠缺血/再灌注心肌的保护作用

目的 观察缺血后处理对高血脂大鼠缺血/再灌注（I/R）心肌的保护作用。方法 选择高血脂SD大鼠36只,随机分为3组,即假手术组、I/R组和缺血后处理组,每组12只。制备大鼠心肌I/R模型。I/R组:收紧结扎线缺血40 min,放松结扎线再灌注240 min。缺血后处理组:缺血40 min后,再灌注10 s,缺血10 s,连续3个循环,然后再灌注240 min。假手术组:开胸后穿线做套环,但不收紧结扎线。用全自动生化仪测定血清肌酸激酶（CK）的含量,黄嘌呤氧化酶法检测超氧化物岐化酶（SOD）的活性。采用硫代巴比妥酸法测定丙二醛（MDA）的含量,用伊文氏蓝-红四氮唑（TTC）染色法测定心肌梗死的范围。结果 ①血清CK活性的测定:再灌注结束后,缺血后处理组和I/R组的活性CK的活性明显高于假手术组［分别为（712.94±20.68）、（946.58±27.43） vs （232.12±18.26）U/L,P<0.05,1 U=16.67 nkat］,缺血后处理组明显低于I/R组(P<0.05)。②血清SOD和MDA的含量:缺血后处理组血清SOD 的含量高于对照组(P<0.05);MDA的含量明显低于对照组(P<0.05)。③心肌梗死范围:再灌注结束后,缺血后处理组和I/R组的心肌缺血区与左室面积的比率无明显差异。缺血后处理组的心肌坏死区与缺血区的比率显著低于I/R组［分别为(25.3±6.6）% vs （39.2±7.1）%,P<0.05］。结论 缺血后处理对高血脂大鼠I/R心肌具有保护作用。     

曲美他嗪后处理与缺血后处理对大鼠再灌注心肌保护作用的对比

目的 对比观察曲美他嗪(TMZ)后处理与缺血后处理(IPOC)对大鼠心肌缺血再灌注损伤(MIRI)的保护作用.方法40只Wistar 大鼠随机分为4组(n=10):假手术组、模型组、曲美他嗪组(TMZ组)、缺血后处理组(IPOC组).结扎左冠状动脉前降支,建立大鼠心肌缺血/再灌注损伤模型,记录各组心肌梗死面积,光镜HE染色观察心肌组织细胞形态,透射电镜观察心肌细胞微观结构,测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(AST)活性变化.结果 TMZ组、IPOC组与模型组比较:①心肌梗死面积减少(P＜0.05);②心肌细胞损伤程度相当,较模型组有明显改善;③心肌细胞超微结构损伤程度相当,较模型组有明显改善;④心肌酶CK、LDH、AST活性较模型组均有明显降低(P＜0.05).结论 TMZ后处理与IPOD对MIRI心肌均有明显的保护作用,二者作用差异不明显.     

肢体缺血后处理对直接冠状动脉介入治疗心肌再灌注损伤的干预研究

目的:用肢体缺血后处理的方法,干预直接经皮冠状动脉介入治疗(PCI)急性ST段抬高型心肌梗死(STEMI),以减轻心肌缺血再灌注损伤。方法:对拟行直接PCI的急性STEMI患者62例,用随机数字法分为肢体缺血后处理(LIPost)组30例和常规对照(NC)组32例。LIPost组在球囊首次扩张梗死相关血管(IRA)前,用血压计袖带缠绕于上臂并充气达250mmHg(1mmHg=0.133kPa),持续5min后放气,间隔5min后重复1次;NC组不作预处理。比较2组术后IRA心肌梗死溶栓试验血流分级(TIMI)、梗死相关区域(IRZ)心肌呈色分级(MBG)、ST段抬高回落指数(STR)、再灌注心律失常(RA)和心肌钙蛋白I(cTnI)峰值前移的发生率,以及症状至球囊扩张时间(SOTB)。结果:2组患者的主要基线指标无统计学差异。2组患者IRA前向血流达TIMI 3级和cTnI峰值前移的获得率相似(96.7%∶96.9%,P=1.000;93.3%∶84.4%,P=0.476),差异无统计学意义。与NC组相比,LIPost组MBG≥2级和STR≥50%获得率较高(80.0%∶56.3%,P=0.046;83.3%...     

The mitochondrial permeability transition pore as a target for preconditioning and postconditioning

The experimental evidence supporting the mitochondrial permeability transition pore (mPTP) as a major mediator of lethal myocardial reperfusion injury and therefore a critical target for cardioprotection is persuasive. Although, its molecular identity eludes investigators, it is generally accepted that mitochondrial cyclophilin-D, the target for the inhibitory effects of cyclosporine-A on the mPTP, is a regulatory component of the mPTP. Animal myocardial infarction studies and a recent clinical proof-of-concept study have demonstrated that pharmacologically inhibiting its opening at the onset of myocardial reperfusion reduces myocardial infarct size in the region of 30–50%. Interestingly, the inhibition of mPTP opening at this time appears to underpin the infarct-limiting effects of the endogenous cardioprotective strategies of ischemic preconditioning (IPC) and postconditioning (IPost). However, the mechanism underlying this inhibitory action of IPC and IPost on mPTP opening is unclear. The objectve of this review article will be to explore the potential mechanisms which link IPC and IPost to mPTP inhibition in the reperfused heart.     

Remote ischemic postconditioning protects against gastric mucosal lesions in rats

AIM: To investigate the protective effects of remote ischemic postconditioning (RIP) against limb ischemia-reperfusion (IR)-induced gastric mucosal injury.METHODS: Gastric IR was established in male Wistar rats by placing an elastic rubber band under a pressure of 290-310 mmHg on the proximal part of both lower limbs for 3 h followed by reperfusion for 0, 1, 3, 6, 12 or 24 h. RIP was performed using three cycles of 30 s of reperfusion and 30 s of reocclusion of the femoral aortic immediately after IR and before reperfusion for up to 24 h. Rats were randomly assigned to receive IR (n = 36), IR followed by RIP (n = 36), or sham treatment (n = 36). Gastric tissue samples were collected from six animals in each group at each timepoint and processed to determine levels of malondialdehyde (MDA), superoxide dismutase (SOD), xanthine oxidase (XOD) and myeloperoxidase (MPO). Additional samples were processed for histologic analysis by hematoxylin and eosin staining. Blood samples were similarly collected to determine serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), tumor necrosis factor (TNF)-α and interleukin (IL)-10.RESULTS: The pathologic changes in gastric tissue induced by IR were observed by light microscopy. Administration of RIP dramatically reduced the gastric damage score after 6 h of reperfusion (5.85 ± 0.22 vs 7.72 ± 0.43; P < 0.01). In addition, RIP treatment decreased the serum activities of LDH (3.31 ± 0.32 vs 6.46 ± 0.03; P < 0.01), CK (1.94 ± 0.20 vs 4.54 ± 0.19; P < 0.01) and the concentration of TNF-α (53.82 ± 0.85 vs 88.50 ± 3.08; P < 0.01), and elevated the concentration of IL-10 (101.46 ± 5.08 vs 99.77 ± 4.32; P < 0.01) induced by IR at 6 h. Furthermore, RIP treatment prevented the marked elevation in MDA (3.79 ± 0.29 vs 6.39 ± 0.81) content, XOD (7.81 ± 0.75 vs 10.37 ± 2.47) and MPO (0.47 ± 0.05 vs 0.82 ± 0.03) activities, and decrease in SOD (4.95 ± 0.32 vs 3.41 ± 0.38; P < 0.01) activity in the gastric tissue as measured at 6 h.CONCLUSION: RIP provides effective functional protection and prevents cell injury to gastric tissue induced by limb IR via anti-inflammatory and antioxidant actions.     

Persistent beneficial effect of postconditioning against infarct size: role of mitochondrial K<Subscript>ATP</Subscript> channels during reperfusion

This study tested the hypothesis that inhibition of myocardial injury and modulation of mitochondrial dysfunction by postconditioning (Postcon) after 24 h of reperfusion is associated with activation of K(ATP) channels. Thirty dogs undergoing 60 min of ischemia and 24 h of reperfusion (R) were randomly divided into four groups: Control: no intervention at R; Postcon: three cycles of 30 s R alternating with 30 s re-occlusion were applied at R; 5-hydroxydecanoate (5-HD): the mitochondrial K(ATP) channel blocker was infused 5 min before Postcon; HMR1098: the sarcolemmal K(ATP) channel blocker was administered 5 min before Postcon. After 24 h of R, infarct size was smaller in Postcon relative to Control (27 +/- 4%* Vs. 39 +/- 2% of area at risk), consistent with a reduction in CK activity (66 +/- 7* Vs. 105 +/- 7 IU/g). The infarct-sparing effect of Postcon was blocked by 5-HD (48 +/- 5%(dagger)), but was not altered by HMR1098 (29 +/- 3%*), consistent with the change in CK activity (102 +/- 8(dagger) in 5-HD and 71 +/- 6* IU/g in HMR1098). In H9c2 cells exposed to 8 h hypoxia and 3 h of reoxygenation, Postcon up-regulated expression of mito-K(ATP) channel Kir6.1 protein, maintained mitochondrial membrane potential and inhibited mitochondrial permeability transition pore (mPTP) opening evidenced by preserved fluorescent TMRE and calcein staining. The protective effects were blocked by 5-HD, but not by HMR1098. These data suggest that in a clinically relevant model of ischemia-reperfusion (1) Postcon reduces infarct size and decreases CK activity after prolonged reperfusion; (2) protection by Postcon is achieved by opening mitochondrial K(ATP) channels and inhibiting mPTP opening. *P < 0.05 Vs. Control; (dagger) P < 0.05 Vs. Postcon.     

远距缺血后适应对缺血再灌注心肌的保护作用

目的:探讨远距缺血后适应(RIP)对兔局部短期缺血再灌注心肌的保护作用.方法:将24只新西兰白兔随机平均分成4组:假手术对照组(S组)、缺血再灌注对照组(IR组)、缺血后适应组(Post组)、RIP组.采用TUNEL分析检测各组心肌组织的细胞凋亡情况,Western blot方法检测Bcl-2、Bax蛋白的表达.结果:...     

线粒体通透性转换孔在精脒介导的心肌缺血再灌注损伤中的作用

目的:研究线粒体通透性转换(PT)孔在精脒介导的心肌缺血/再灌注损伤中的作用。方法:采用Langendorff灌流离体大鼠心脏,全心停灌30min,复灌120min造成心肌缺血复灌模型。采用高效液相色谱法测定心肌组织精脒含量;复灌前10min给予不同浓度精脒,记录左室收缩压(LVSP)、左室压上升/下降最大速率(±dp/dtmax)和左室舒张末期压力(LVEDP);用紫外分光光度法检测复灌10min的冠状动脉(冠脉)流出液乳酸脱氢酶(LDH)活性;用TTC染色法测心肌梗死面积。检测不同浓度精脒对心肌线粒体PT孔开放改变(520nm吸光度变化)。结果:与对照组比较,大鼠心肌缺血期及再灌期精脒含量均减少(P<0.05);与单纯缺血/复灌组相比,于复灌前10min给予线粒体通透性转换孔特异性阻断剂环孢菌素A(CsA 0.2mol/L)和精脒(0.1mol/L、1μmol/L、5μmol/L),左室收缩舒张功能改善,其中LVSP上升(P<0.01),LVEDP下降(P<0.01),±dp/dtmax提高(P<0.01);冠脉流出液中LDH含量明显减少(P<0.01),梗死面积减少(P<0.01)。而于复灌前10min给予精脒(10μmol/L,15μmol/L),与单纯缺血/复灌组比较,LVSP均明显下降(均P<0.01),LVEDP明显上升(P<0.01),±dp/dtmax下降(P<0.01);复灌10min后冠脉流出液中LDH含量明显增加(P<0.01),梗死面积均增加(均P<0.01);在分离的线粒体给予精脒,高浓度PT孔开放幅度增加;低浓度开放受到抑制。结论:精脒可通过抑制或增强线粒体PT孔开放而对缺血/再灌心肌产生保护或加重损伤的作用。     

心肌缺血后适应的保护作用及机制研究进展

急性心肌梗死发病率的增高,促进了再灌注治疗如溶栓及经皮冠脉介入治疗的应用.这却引起了心肌细胞死亡、血流动力学障碍、再灌注心律失常及内皮功能障碍等缺血再灌注损伤[1].众多研究证实,缺血后适应对缺血再灌注损伤心肌具有保护作用,能够降低梗死面积[2]、减少细胞凋亡[3]、改善内皮功能[4]及减轻组织的水肿[4]等.缺血后适应,即在心肌缺血再灌注的即刻对冠脉进行短暂、重复的开通及再闭过程,随后恢复冠状动脉血流[4].后适应的可操作性,决定了其在临床中应用的可能性.本文就后适应在心肌缺血再灌注损伤中的保护应用及其机制进行综述.     

芬太尼后处理联合缺血后适应对兔心肌缺血再灌注损伤心肌坏死标志物的影响

目的 观察芬太尼后处理联合缺血后适应对兔心肌缺血再灌注损伤心肌坏死标志物及心肌梗死面积的变化,探讨其对心肌缺血再灌注损伤的保护作用.方法 32只日本大耳白兔,采用结扎左冠状动脉前降支30 min、复灌120 min建立心肌缺血再灌注损伤模型.按“随机数字表法”随机分为4组,每组8只：假手术组,动脉下仅穿线不结扎;缺血再灌注组,直接恢复再灌注;缺血后适应组,缺血后适应后恢复再灌注;芬太尼后处理＋缺血后适应组,缺血28 min给予芬太尼5μg· kg-1后处理,30 min予以缺血后适应.测定各组心肌坏死标志物（心肌肌钙蛋白Ⅰ浓度与肌酸激酶同工酶蛋白活力浓度）、计算心肌梗死面积及观察室性心律失常发生率.结果 芬太尼后处理＋缺血后适应组较缺血后适应组、缺血再灌注组外周血心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度降低,心肌梗死面积减小,差异均有统计学意义（P＜0.05）.缺血后适应组较缺血再灌注组外周血心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度降低,心肌梗死面积减小,差异均有统计学意义（P＜0.05）.芬太尼后处理＋缺血后适应组、缺血后适应组较缺血再灌注组室性心律失常发生率降低[0 vs.50％（4/4）,P＜0.05;12.5％（1/7）vs.50％（4/4）,P＜0.05],差异均有统计学意义（P＜0.05）.结论 芬太尼后处理联合心肌缺血后适应显著降低兔心肌缺血再灌注心肌肌钙蛋白Ⅰ浓度、肌酸激酶同工酶酶蛋白活力浓度,减少心肌梗死面积,降低室性心律失常发生率,可减轻心肌缺血再灌注损伤.     

Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditioning’s success

Repetitive cycles of reflow/reocclusion in the initial 2 min following release of a prolonged coronary occlusion, i.e., ischemic postconditioning (IPoC), salvages ischemic myocardium. We have proposed that the intermittent ischemia prevents formation of mitochondrial permeability transition pores (MPTP) by maintaining an acidic myocardial pH for several minutes until survival kinases can be activated. To determine other requisites of IPoC, isolated rabbit hearts were subjected to 30 min of regional myocardial ischemia and 120 min of reperfusion. Infarct size was determined by staining with triphenyltetrazolium chloride. During the first 2 min of reperfusion the perfusate was either at pH 7.4 following equilibration with 95% O(2)/5% CO(2), pH 6.9 following equilibration with 80% N(2)/20% CO(2), or pH 7.8 following equilibration with 100% O(2). Whereas acidic, oxygenated perfusate for the first 2 min of reperfusion was cardioprotective, protection was lost when acidic perfusate was hypoxic. However, the acidic, hypoxic hearts could be rescued by addition of phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, to the perfusate. Therefore, both low pH and restoration of oxygenation are necessary for protection, and the signaling step requiring combined oxygen and H(+) must be upstream of PKC. To gain further insight into the mechanism of IPoC, the latter was effected with 6 cycles of 10-s reperfusion/10-s reocclusion. Its protective effect was abrogated by either making the oxygenated perfusate alkaline during the reperfusion phases or making the reperfusion buffer hypoxic. Presumably the repeated coronary occlusions during IPoC keep myocardial pH low while the resupply of oxygen during the intermittent reperfusion provides fuel for the redox signaling that acts to prevent MPTP formation even after restoration of normal myocardial pH. Hearts treated simultaneously with IPoC and alkaline perfusate could not be rescued by addition to the perfusate of either PMA or SB216763 which inhibits GSK-3beta, the putative last cytoplasmic signaling step in the signal transduction cascade leading to MPTP inhibition. Yet cyclosporin A which also inhibits MPTP formation does rescue hearts made alkaline during IPoC. In view of prior studies in which the ROS scavenger N-2-mercaptopropionyl glycine aborts IPoC's protection, our data reveal that IPoC's reperfusion periods are needed to support redox signaling rather than improve metabolism. The low pH, on the other hand, is equally necessary and seems to suppress MPTP directly rather than through upstream signaling.     

缺血后处理对大鼠移植心脏心肌缺血再灌注损伤不同时相的保护作用

目的探讨缺血后处理对大鼠移植心脏心肌缺血再灌注损伤不同时相的保护作用。方法建立近交系Lewis大鼠颈部异位心脏移植左心做功模型,受体大鼠存活2d后,随机分为3组:缺血再灌注组:结扎移植心脏冠状动脉左前降支30 min后再灌注3h、6h、12h、24h、2d、4d及7d,每个时相点8只受体鼠;缺血后处理组:移植心脏缺血30 min,在再灌注前1 min给予再通10秒,阻断10秒,连续3个循环。每个时相点8只受体鼠;假手术组:穿线做套环,但不收紧结扎线。分别比较再灌注结束后大鼠血清肌酸激酶同工酶MB(CK-MB)值、移植心脏心肌细胞凋亡指数和梗死范围。结果在再灌注时间3h、6h、12h、24h、2d、4d 6个时相点,缺血再灌注组与缺血后处理组血清CK-MB均值对应比较,差异均有统计学意义(P均0.05),均明显高于假手术组CK-MB值(P均0.05)。再灌注6h时,缺血后处理组CKMB峰值较缺血再灌注组明显降低[(34.73±8.83)U/L vs.(52.58±10.05)U/L,P0.01]。在再灌注时间3h、6h、12h、24h、2d、4d、7d 7个时相点,缺血后处理组心肌细胞凋亡指数及心肌梗死范围均低于缺血再灌注组,差异均有统计学意义(P均0.05),心肌细胞凋亡指数均高于假手术组(P均0.05)。结论缺血后处理在大鼠移植心脏心肌缺血再灌注3h~7d内能降低血清CK-MB峰值,减少心肌细胞凋亡和心肌梗死范围。