兔右冠脉缺血预适应与右心缺血再灌注损伤

目的 :探讨兔右冠脉缺血预适应 (IP)与缺血再灌注损伤 (IR)的相关性。方法 :以单纯缺血 6 0 min 再灌注 6 0 min(IR)为对照 ,观察经 IP(缺血 5min 再灌注 10 min)后 IR心肌缺血型 S- T段、超微结构改变及再灌注心律失常发生率。结果 :较之 IR组 ,IP组的 ST段明显下移 ,电镜下见右室和右房心肌超微结构改变明显减轻 ,缓慢型再灌注心律失常的发生率明显减少。结论 :清醒兔右冠脉 IP可减少 IR引起的右心缺血性超微结构损伤及再灌注心律失常发生率     

缺血预适应对心室颤动阈影响的研究

目的探讨兔右冠状动脉缺血预适应(ischemicpreconditioning,IP)对心室肌心室颤动阈的影响。方法根据顺序单脉冲刺激原理,采用RS2程序电刺激法,测量缺血再灌注组(IR组)(I30min+R30min)及缺血预适应(IP组)(I5min+R10min+I30min+R30min)在缺血30min(I30min)内及再灌注30min(R30min)内心室颤动阈(VFT)变化,并与正常对照组比较。结果①IR组及IP组于I30min内缺血心室肌VFT与正常对照组比较,VFT较低,差别有显著性(P＜0.01);与正常对照组比较,IR组于R30min内缺血心室肌VFT较低,差别有显著性(P＜0.01),但IP组同时期上述指标与正常对照组差异无显著性(P＞0.05);②IP组缺血心室肌于I30min、R30min内与IR组比较,VFT升高,差异有显著性(P＜0.01);③左心室IR组及IP组VFT与右心室相应指标比较,VFT较高,差异有显著性(P＜0.01)。结论右冠状动脉IP可提高缺血及再灌注心室肌的心室颤动阈。     

缺血预适应对大鼠肺缺血再灌注中NF-κB表达的影响

目的研究缺血预适应(IP)对缺血再灌注(I/R)后在体鼠肺脏NFκB表达的影响,探讨IP减轻肺脏I/R损伤的可能机制及NFκB的作用。方法雄性SD大鼠36只,随机分为3组假手术(Sham)组,缺血再灌注(I/R)组,缺血预适应(IP)组。I/R组开胸后,建立在体肺脏I/R损伤模型。在此基础上,IP组于缺血开始前,应用3个循环的5min缺血 5min灌注进行IP处理。用免疫组化法观察肺脏NFκB的表达,同时测定肺脏湿重/干重(W/D)比值,电镜下观察肺脏超微结构的改变,光镜下HE染色观察肺脏的病理形态学变化。结果IP组和I/R组相比肺脏NFκB表达有显著性差异(P<0.01),肺脏超微结构损害和肺水肿程度明显减轻。结论IP可抑制I/R损伤时肺组织中NFκB的表达,从而减轻肺脏超微结构损害和肺水肿程度,减轻肺I/R损伤。     

缺血预处理对缺血再灌注窦房结细胞凋亡及bcl-2和bax基因表达的影响

目的:探讨体内兔右冠状动脉缺血预处理(IP),对缺血再灌注(IR)窦房结细胞凋亡及bcl-2、bax蛋白表达和再灌注心律失常发生的影响。方法:体内兔右冠状动脉根部结扎或放松制作窦房结IR和IP模型。健康成年新西兰兔30只分3组:假手术组,IR组,IP组。记录再灌注心律失常发生并检测窦房结细胞凋亡指数(AI)及bcl-2、bax蛋白表达的积分吸收度(A)值。结果:①IP组再灌注心律失常发生较IR组明显减少;②IP组较IR组AI值均显著下降(P<0.01),bcl-2蛋白表达明显增多(P<0.01),而bax蛋白表达量低(P<0.05)。结论:IP减少因IR所致的窦房结细胞凋亡,其机制可能与上调bcl-2和下调bax蛋白表达相关。     

缺血预处理对在体家兔房室结细胞形态结构的影响

目的观察缺血预处理在家兔急性心肌梗死模型中,对在体房室结细胞形态结构的影响.方法健康家兔30只,雌雄不拘,随机分为假手术组,缺血再灌注(IR)A组、B组,缺血预处理(IP)A组、B组,通过结扎右冠状动脉建立家兔房室结缺血再灌注模型,观察经过缺血预处理后,以不同的再灌注时间30 min(A组)、180 min(B组)为实验终点,检测心脏血心肌酶变化,HE染色和透视电镜观察房室结细胞的形态学变化.结果IP组较IR组心肌酶检测值显著降低,光镜下细胞空泡变性及细胞坏死IP组较IR组明显减轻.电镜下房室结细胞的线粒体、肌丝等超微结构在IP组损伤也明显减轻.结论缺血预处理对房室结细胞有保护作用.     

模拟缺血-再灌注对窦房结细胞起搏离子流的影响及K_(ATP)通道开放剂的干预作用

探讨模拟缺血 再灌注对窦房结细胞起搏离子流 (If)的影响及KATP通道开放剂Pinacidil的干预效果。分离乳鼠窦房结细胞 ,纯化培养 2天后进行实验。随机分为对照组、模拟缺血 再灌注组 (I/R)、KATP通道开放剂Pinacidil干预组 (P +I/R)及KATP通道阻断剂 5 HD干预组 (5 HD +P +I/R及 5 HD +I/R)。采用常规全细胞膜片钳技术及多导管灌流系统 ,测定各组细胞If 密度 ,并绘制If 激活曲线。结果 :①每个窦房结细胞均可记录到If 电流 ,在相同指令电压下 ,I/R组窦房结细胞If 密度值较对照组明显增加 (P <0 .0 1) ;而P +I/R组则较I/R组显著减小 (P <0 .0 1) ;5 HD +P +I/R及 5 HD +I/R两组又较P +I/R组明显增加 (P <0 .0 1) ,但与I/R组比较无显著差异。②与对照组比较 ,I/R组窦房结细胞的If 激活曲线发生右移 ,半数最大激活电压由 - 10 8.0± 12 .4mV变为 - 89.5± 7.2mV(P <0 .0 1) ;P +I/R组窦房结细胞If 激活曲线较I/R组左移 ,半数最大激活电压为 - 99.5± 10 .8mV(P <0 .0 5 ) ;KATP通道阻断剂 5 HD可阻断Pinacidil对If 激活曲线的影响。结论 :KATP通道开放剂Pinacidil可对抗模拟缺血 再灌注对窦房结细胞If 的影响 ,此有利于维持模拟缺血 再灌注时窦房结细胞离子稳态和电生理活动的相对稳定     

缺血再灌注时心肌细胞凋亡情况及去甲肾上腺素预处理对其影响

目的　探讨微量去甲肾上腺素预处理对大鼠缺血再灌注心肌细胞凋亡的影响。方法　大鼠在体缺血再灌注 (I/ R)模型 ,分别以缺血前去甲肾上腺素预处理 (NE- P) ,缺血预处理 (IP) ;采用末端脱氧核苷酸转换酶介导的生物素平移缺口末端标记技术 (TUNEL )检测各组心肌细胞凋亡情况及心肌梗死范围。结果　 I/ R组细胞凋亡率 (43.33%± 4.92 % )较高 ,NE- P组及 IP组虽然也有一定的心肌细胞凋亡率 :2 5.2 4 %± 1 .56% ,2 4 .44%± 2 .96% ,但较 I/ R组明显降低 (P<0 .0 0 1 )。 IP组及 NE- P组心肌梗死范围较 I/ R组明显减少 ,IP组及 NE- P组两项指标无显著差异。结论　心肌缺血再灌注损伤可诱发心肌细胞凋亡 ,NE- P能明显减少缺血再灌注诱导的心肌细胞凋亡的发生率 ,能明显减少心肌梗死范围 ,减轻缺血再灌注损伤 ;NE- P减少心肌梗死范围、减轻缺血再灌注损伤的机制可能与其能明显减少心肌细胞凋亡有关。     

缺血再灌注对在体兔窦房结细胞凋亡影响的研究

探讨缺血再灌注对在体兔窦房结细胞凋亡的影响。取家兔 90只随机分为对照组 ,缺血 10 ,30 ,6 0 ,12 0min组及缺血 10 ,30 ,6 0 ,12 0min再灌注 4h组 ,每组 10只。通过结扎及放松右冠状动脉起始部制作窦房结缺血再灌注损伤模型 ,当达各预定时间点后 ,迅速切取窦房结组织固定 ,用TUNEL法检测窦房结细胞凋亡。结果 :①对照组、缺血10 ,30min组均未观察到明显的窦房结细胞凋亡现象。②缺血 6 0 ,12 0min组及缺血再灌注 4组中共有 6 8.3% (41/6 0 )的兔子窦房结细胞出现不同程度的凋亡现象 ,表明该部分兔子的窦房结动脉起源于右冠状动脉。③缺血 6 0 ,12 0min两组窦房结细胞凋亡率分别为 8.6 %与 16 .1% ,而缺血 10 ,30 ,6 0 ,12 0min再灌注 4h 4组中窦房结细胞凋亡率分别为 2 3.5 %、34.5 %、4 4 .7%与 31.2 %。结论 :缺血再灌注可诱导在体兔窦房结细胞凋亡 ,且随缺血时间延长 ,细胞凋亡率逐渐增加 ;再灌注组细胞凋亡率较相同时间缺血组明显增加 ,表明缺血再灌注损伤介导了窦房结细胞凋亡。     

细胞骨架在原代培养乳鼠窦房结细胞模拟缺血预适应中的作用研究

观察细胞骨架在乳鼠窦房结细胞模拟缺血预适应(IP)中的作用。取培养 2d的乳鼠窦房结细胞,随机分为①对照组;②模拟缺血 /再灌注(I/R)组;③模拟IP组;④phalloidin(微丝聚合剂 ) +I/R组;⑤cytochalasinD(微丝解聚剂) +IP组:⑥Taxol(微管聚合剂 ) +I/R组;⑦colchicine(微管解聚剂 ) +IP组。以FITC phalloidin及SABC cy3试剂盒分别标记F actin及β tubulin,用激光共聚焦显微镜检测各组窦房结细胞荧光强度改变。结果:①phalloi din预处理能显著增强再灌注后窦房结细胞F actin及β tubulin的荧光强度,并维持其形态、结构的相对完整性,模拟IP效应。②cytochalasinD及colchicine均能阻断模拟IP的细胞骨架保护作用,显著降低窦房结细胞F actin及β tubulin的荧光强度,导致细胞骨架的解体。③Taxol未能对I/R窦房结细胞提供IP样保护作用。结论:维持微丝结构的相对完整性可以减轻窦房结细胞I/R损伤,模拟IP效应;维持细胞骨架的相对完整性是IP产生的重要前提。     

大白兔肝缺血再灌注损伤时血浆内毒素的变化及对肝肾功能的影响

目的探讨肝缺血再灌注损伤过程中,肠源性内毒素的动态变化和继发性肝肾功能损害。方法取27只健康成年新西兰大白兔,体重1.4~2.3?,随机分为对照组7只,另外20只作为实验组。以缺血10min(I10min)、缺血20min(I20min)、缺血30min(I30min)和分别再灌注30min(R30min)随机分为3组。对照组取门、腔静脉血测肝肾功能及血浆内毒素,实验组阻断第一肝门造成不同的缺血时段,松开血管夹再灌注30min,其余实验同对照组。结果实验组中血浆谷草转氨酶、谷丙转氨酶、尿素氮、肌苷含量及内毒素浓度均有升高,在I10min/R30min组即有升高,但与对照组相比差异无显著性(P>0.05);而后随着缺血时间的延长这些指标继续明显升高,至I30min/R30min组达最高值,与对照组比差异有显著性(P<0.05~0.01)。肾组织电镜观察发现I10min/R30min组肾脏超微结构无明显改变,而I20min/R30min组和I30min/R30min组肾脏超微结构损害明显。结论肝门阻断后门静脉系统淤血,致肠源性内毒素产生和移位;肝门再开放造成肝缺血再灌注损伤,且随着缺血时间的延长,门、腔静脉血中内毒素水平进行性升高,肝功能进一步损害,最终引起肝肾综合征。     

兔右冠状动脉急性闭塞与再灌注时心律失常的发生与演变

为观察右冠状动脉急性闭塞时与再灌注时心律失常的发生及演变 ,取家兔 90只随机分为对照组、缺血 1 0 ,30 ,60 ,1 2 0min组及缺血 1 0 ,30 ,60 ,1 2 0min再灌注 4h组 ,每组 1 0只。通过结扎及放松右冠状动脉起始部建立缺血再灌注损伤模型 ,同步记录体表心电图及His束电图 ,观察AA、AH、HV间期的变化及心律失常发生与演变情况。结果 :①对照组各时相点AA、AH、HV间期比较均无显著差异 (P >0 .0 5)。②实验组 80只兔中 ,结扎右冠状动脉后 3只 (3 .75 % )发生心室颤动、67只 (83 .75 % )发生不同程度的房室阻滞 ,51只 (63 .75 % )发生窦性及房性心律失常 ,54只 (占 67.5 % )的AA间期延长在 40ms以上。③缺血再灌注组 40只兔 ,2 6只于缺血期发生窦性或房性心律失常 ,其中 1 5只于再灌注后 2 0min内恢复正常 ;缺血时发生房室阻滞的 7只兔均于再灌注后 30min内逐渐恢复正常。另有 3只发生了新的心律失常。④缺血期出现AA、AH间期延长的兔 ,均于再灌注后短期内迅速缩短 ,并逐渐恢复至对照组水平 ;但缺血 1 2 0min再灌注组 ,则随着再灌注时间进一步延长 ,AA及HV间期再次延长。结论 :右冠状动脉急性闭塞可引起兔窦房结放电频率减慢及房室传导障碍 ,再灌注后多数可于短期内迅速恢复 ,但较长时间缺血后再灌注可发生     

神经型一氧化氮合酶在小鼠心肌缺血预处理中的作用

目的 应用神经型一氧化氮合酶(nNOS)基因敲除小鼠和nNOS抑制剂,探讨nNOS对心肌缺血预处理后心肌细胞凋亡的影响.方法 实验分为野生型缺血再灌注组(WT IR)、野生型缺血预处理组(WT IP)、野生型缺血预处理L-VNIO处理组(WT IP+ L-VNIO)、基因敲除鼠缺血再灌注组(KO IR)和基因敲除鼠缺血预处理组(KO IP).采用冠状动脉左前降支结扎法建立小鼠缺血再灌注损伤模型,缺血再灌注组缺血30 min再灌注3h,缺血预处理组分别经缺血5 min再灌注5 min连续三个循环后,再缺血30 min再灌注3h,观察TUNEL染色和Caspase-8、Caspase-9、Caspase-3的活性变化,并用Western Blot法观察Bax、Bcl-2和Fas蛋白的表达情况.结果 与WT IR组相比,WT IP组小鼠TUNEL阳性细胞数目减少,Caspase-8、Caspase-9和Caspase-3活性降低,Bax和Fas蛋白表达显著降低,Bcl-2表达显著增加(P＜0.05).而在KO IP组,与KO IR组相比,TUNEL阳性细胞数目和Caspase活性显著增加,Bax和Fas表达显著增高,Bcl-2表达显著降低(P＜0.05).结论 nNOS在心肌缺血预处理时发挥抑制心肌细胞凋亡的作用.     

Protective effects of ischemic preconditioning on lung ischemia reperfusion injury: an in-vivo rabbit study

BACKGROUND: The goal of this study was to determine the effect of ischemic preconditioning on the extent of normothermic lung ischemia reperfusion injury in rabbits in vivo. METHODS: Thirty male Japanese white rabbits were randomized into two groups. Fifteen rabbits were treated with ischemic preconditioning (their left lung hilus clamped for 10 minutes and released for 15 minutes (group IP)). Fifteen rabbits were not treated with ischemic preconditioning (group C). Then the left lung hilus of both groups were occluded for 60 minutes and reperfused for 60 minutes. Mean arterial pressure, mean pulmonary artery pressure, and core temperature were recorded. Femoral artery blood samples and lung tissue samples were collected after ischemic preconditioning and after 60 minutes of reperfusion. RESULTS: The lung tissue showed little injury after ischemic preconditioning. After 60 minutes of reperfusion, the angiotensin II (A II) and arterial oxygen tension (PaO2) levels in group IP were significantly higher than those in group C, mean pulmonary artery pressure in group IP was significantly lower than that in group C, the wet/dry ratio and malondialdehyde content of lung tissue in group IP was significantly lower than that in group C, the superoxide dismutase contents of lung tissue in group IP was significantly higher than that in group C, and histological findings showed less damage in group IP than in group C. CONCLUSION: Lung ischemic preconditioning could reduce normothermic rabbit lung ischemia-reperfusion injury. The possible mechanisms are increased production of endogenous A II and reduced formation of oxygen free radicals during lung ischemia for 60 minutes followed by reperfusion for 60 minutes.     

诱导型一氧化氮合酶和解偶联蛋白-2对心肌缺血预适应的作用

目的 探讨诱导型一氧化氮合酶（inducible nitric oxide synthase,iNOS）和解偶联蛋白-2（uncoupling protein-2，UCP2）对大鼠心肌缺血预适应的保护机制。方法 结扎左冠状动脉复制大鼠心肌缺血再灌注模型。预适应组行3次缺血5min，再灌注10min的预处理，分别于预处理0，6，12，24和48h（分别为0，6，12，24和48h亚组）后行30min缺血及120min再灌注：对照组开胸后不结扎左冠状动脉，电镜观察心肌超微结构，据Rainio评分标准进行心肌超微结构损伤程度的半定量分析。采用Western Blot及比色法检测心肌UCP2活性及iNOS活性。结果 预适应各亚组UCP2活性均增高（P〈0．05），0h亚组UCP2表达水平最高（P〈0．01），24小时亚组和48小时亚组心肌iNOS活性显著升高（P〈0．05）。结论 UCP2和iNOS共同参与了大鼠心肌缺血预适应心肌保护作用。     

Effects of ischemic preconditioning on cyclinD1 expression during early ischemic reperfusion in rats

AIM: To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion. METHODS: Fifty-four SD rats were randomly divided into ischemic preconditioning group (IP), ischemia/ reperfusion group (IR) and sham operation group (SO). The IP and IR groups were further divided into four sub-groups (n - 6). Sham operation group (SO) served as the control group (n = 6). A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. After 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinDi mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS: Compared with IR group, IP group showed a significantly lower ALT level in 1 h to 4 h sub-groups (P < 0.05). Proliferation index(PI) indicated by the S-phase and G2/M-phase ratio [(S G2/M)/(G0/G1 S G2/M)] was significantly increased in IP group at 0 and 1 h (26.44±7.60% vs 18.56±6.40%,41.87±7.27% vs 20.25±6.70%, P < 0.05). Meanwhile, cyclinDi protein expression could be detected in IP group. But in IR group, cyclinDi protein expression occurred 2 h after reperfusion. The expression of cyclinDi mRNA increased significantly in IP group at 0 and 1 h (0.568±0.112 vs 0.274±0.069, 0.762±0.164 vs 0.348±0.093, P < 0.05). CONCLUSION: Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion.     

后肢远程预处理对心肌缺血再灌注与心交感神经损伤的影响

目的：后肢远程缺血预处理对急性心肌缺血再灌注与心交感神经损伤影响的实验研究。方法：20只雄性新西兰大白兔随机被均分成两组：对照组及远程缺血预处理（RIPC）组。两组均制作心肌缺血模型。RIPC组在心肌缺血前行双后肢短暂缺血预处理2次（充气式压力止血带环扎双后肢腘窝上1／3,压力26．6kPa,每次10min,间隔10min）,最后一次后肢缺血预处理后再灌注60min制作急性心肌缺血模型。其方法为：冠状动脉左前降支完全闭塞45min,于松开结扎圈再灌注2、4h时,分别以碘-间位碘代苄胍（^131-MIBG）、^99m锝-甲氧基异丁基异腈（^99mTc-MIBI）双核素作放射自显影,其后以美蓝、氯化四唑（TTC）作组织染色,分别确定心肌危险梗塞灶与实际梗塞灶。结果：再灌注4h后,预处理组危险梗塞灶与实际梗塞灶均小于对照组（P〈0．01）。^131I-MIBG及^99m～Tc-M1BI自显影在同一区域摄取存在差异性,两组^131I-MIBG显影缺损面积（40．8土3．2）％．均显著比^99mTc-MIBI显影缺损及实际梗塞灶大（P〈0．05）。结论：远程预处理能有效阻断心肌缺血再灌注对交感神经损伤的作用;利用交感神经显影剂MIBG显影能客观监测心肌梗塞病变范围和程度,评价远程预处理的心肌保护效应。     

贝前列素钠预处理对兔心肌缺血/再灌注损伤的早期拮抗作用

目的:探讨贝前列素钠（beraprost sodium,BPS）预处理对兔心肌缺血/再灌注(I/R)损伤的早期拮抗作用。方法: 将36只日本大耳白兔随机分为3组,即A组（假手术组）、B组（I/R组:缺血40 min后,再灌注90 min）和C组（BPS预处理组:以15 μg/kg,2次/d,［1］连续喂养4周,最后1次喂养后3 h内进行I/R）。以上3组均开胸暴露心脏,A组在左冠状动脉左室支处穿线不结扎,观察130 min结束实验;B组及C组开胸后结扎左冠状动脉左室支40 min,心电图若出现Ⅱ导联ST段升高及结扎周围心肌的颜色变紫或变深显示已形成心肌梗死(MI)模型。然后进行以下检测:①再灌注90 min后,随机选取6只日本大耳白兔,立即取结扎点下损伤的心肌组织,用100 g/L福尔马林固定后,部分进行HE染色在光镜下观察心肌形态学改变;部分用免疫组化染色法检测心肌细胞中Bax、Bcl-2的表达。②再灌注4 h后,取右心房（或股静脉）血应用电化学发光免疫法检测血浆中心肌中肌酸激酶(CK-MB)的变化。结果: ①HE染色显示,A组的心肌结构正常,B组的心肌损伤较严重,C组的心肌损伤较轻。②免疫组化染色法检测显示,A组Bcl-2的表达呈阳性,Bax的表达呈阴性;B组Bax的表达呈强阳性,Bcl-2的表达呈弱阳性;C组Bax的表达呈弱阳性,Bcl-2的表达介于A组与B组之间。③用电化学发光免疫法检测心肌酶学结果,CK-MB升高者3个组依次为B组>C组>A组,B组CK-MB的水平均明显高于C组与A组（P<0.01）。结论: BPS预处理对兔心肌I/R损伤早期具有拮抗作用。     

Preinfarction angina: no interference of coronary microembolization with acute ischemic preconditioning

Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia. Group 2 (n=8) was subjected to coronary microembolization (i.e. microspheres; 42 microm slashed circle; 3000 per ml min-1 inflow) 35 min before sustained ischemia. In group 3, coronary microembolization was followed 10 min later by one cycle of ischemic preconditioning (10 min ischemia/15 min reperfusion) before subsequent sustained ischemia. Infarct size was determined after 2 h reperfusion by triphenyl tetrazolium chloride staining. Infarct size after sustained ischemia alone (group 1) was 19.4+/-3.4% of the area at risk (mean+/-S.E.M.). With coronary microembolization before sustained ischemia (group 2) infarct size was only slightly larger (23.6+/-4.6%, ns). In group 3 with microembolization followed by ischemic preconditioning, infarct size was reduced to 12.7+/-3.0% (P<0.05 vs. group 2). The relationships between infarct size and transmural blood flow in groups 1 and 3 were not different, giving the impression that ischemic preconditioning failed to protect microembolized myocardium. However, additional coronary microembolization shifted the relationship between infarct size and blood flow upwards to a larger infarct size at any given blood flow. Thus when comparing the relationship of group 3 to its true control (group 2), it was shifted downwards (P<0.05; analysis of covariance (ANCOVA)) indicating persistent protection of microembolized myocardium by ischemic preconditioning. Coronary microembolization induces additional infarction when superimposed on sustained ischemia but does not interfere with the endogenous protection by ischemic preconditioning.