低能量氦氖激光血管内照射对缺血再灌注心肌超微结构的影响

目的：探讨低能量氦氖激光血管内照射（ILIB）对缺血再灌注心肌组织超微结构的影响。方法：通过结扎冠状动脉阻断冠状动脉血流，复制家兔急性心肌缺血-再灌注损伤动物模型。将家兔随机分为4组：假手术组、心肌缺血30min组、缺血30min再灌注30min组、缺血30min再灌注30min＋ILIB组。在透射电镜下观察各组心肌超微结构的变化。结果：假手术组心肌纤维呈阶段性收缩、间质水肿、线粒体轻度肿胀、间质可见闭塞的毛细血管；心肌缺血组心肌纤维排列紊乱、肌浆水肿、线粒体水肿、血管扩张、血管结构破坏、血管内可见白细胞镶嵌；缺血再灌注组心肌纤维排列相对整齐、线粒体水肿不明显、肌浆水肿较轻、心肌间质可见轻度毛细血管扩张淤血；缺血再灌注＋ILIB组心肌纤维排列整齐、线粒体无肿胀、间质毛细血管内可见红细胞、无毛细血管内白细胞镶嵌现象、毛细血管管腔通畅、血管壁较完整。结论：ILIB可使缺血再灌注心肌超微结构基本恢复正常，对心肌有保护作用。     

大鼠急性心肌缺血再灌注损伤诱导细胞凋亡的实验研究

目的:观察心肌缺血再灌注(IR)损伤与心肌细胞凋亡关系及凋亡调控基因Bcl-2、Bax表达情况。方法:选用健康雄性SD大鼠29只,随机分为:假手术组(n=8),缺血组(n=12),缺血再灌注组(n=9),分别取上述大鼠心肌组织。(1)观察心肌组织及线粒体的形态结构,并进行体视学分析。(2)采用缺口末端标记法(TUNEL)原位检测凋亡细胞。(3)用免疫组化SP法检测心肌细胞Bcl-2、Bax表达。结果:(1)假手术组心肌纤维排列整齐,细胞间质血管未见明显异常,细胞核膜完整,缺血组及缺血再灌注组可见心肌嗜酸性变、空泡变性、心肌纤维紊乱及收缩带形成,心肌纤维间出血及灶性心肌坏死。心肌细胞线粒体体视学分析,与假手术组比较,心肌缺血组形状因子显著降低(P<0.05),面密度显著增加(P<0.05),缺血再灌注组形状因子显著降低(P<0.01),面密度及周密度均显著增加(均P<0.05)。(2)与假手术组比较,缺血组细胞凋亡率明显升高(P<0.001),缺血再灌注组细胞凋亡率明显升高(P<0.001)。缺血再灌注组与缺血组比较细胞凋亡率明显升高(P<0.05)。(3)与假手术组比较,缺血再灌注组凋亡调控基因Bcl-2、Bax表达明显升高(P<0.01,P<0.001)。缺血再灌注组与缺血组比较凋亡调控基因Bcl-2、Bax表达明显升高(均P<0.01)。结论:心肌缺血及再灌注在导致细胞形态、线粒体超微结构改变的同时,诱导心肌细胞的凋亡,Bcl-2、Bax蛋白表达在心肌细胞凋亡的发生中起重要作用,细胞凋亡加重了缺血再灌注损伤。     

缺血再灌注超早期心肌组织病理改变的实验研究

目的观察缺血再灌注超早期心肌组织的病理变化。方法制备大鼠缺血再灌注模型,观察缺血及再灌注不同时间相心肌组织的病理变化。结果缺血15min时,缺血区心肌细胞水肿、心肌纤维呈不典型的波浪状改变;缺血30min时,可见心肌细胞水肿更加明显,心肌纤维呈明显的波浪状改变;缺血45min时的病理变化与缺血30min时基本相同;再灌注（缺血45min时）后除上述病理变化外,还可发现血细胞在心肌间质中沉积,而且随再灌注时间的延长,血细胞沉积的数量增多。结论缺血及再灌注不同时间相心肌的病理变化有着不同的特点。     

右美托咪定预处理对大鼠心肌缺血再灌注损伤的影响及其机制

目的 观察右美托咪定（Dex）预处理对大鼠心肌缺血再灌注损伤（MIRI）的影响,并探讨其机制是否与氧化应激及Epac1/Rap1信号通路有关。方法 SD大鼠随机分为假手术组、模型组、Dex组、抑制剂组各8只。Dex组在建模前30 min腹腔注射Dex,抑制剂组在建模前30 min及25 min时分别腹腔注射Epac1拮抗剂ESI09及Dex,假手术组、模型组在建模前30 min腹腔注射相同剂量的生理盐水。除假手术组外,各组均通过结扎左冠状动脉建立MIRI模型,假手术组心脏仅穿线而不结扎左冠状动脉。采用苏木精—伊红（HE）染色观察各组心肌组织病理学变化,ELISA法检测大鼠血清心肌损伤标志物肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）及氧化应激指标丙二醛（MDA）、超氧化物歧化酶（SOD）,Western blotting法检测大鼠心肌组织Epac1/Rap1信号通路相关蛋白Epac1、Rap1。结果 假手术组心肌纤维排列整齐、边缘清晰,未见心肌纤维断裂和细胞间质肿胀;模型组心肌纤维出现断裂,排列紊乱、边界模糊,有明显中性粒细胞浸润,细胞间质肿胀明显;Dex组与抑制剂组心肌纤维断裂...     

益气活血法对大鼠心肌缺血再灌注损伤保护作用的实验研究

目的探讨按益气活血法制定的益气活血方对心肌缺血再灌注损伤的保护作用。方法清洁级健康SD大鼠30只,雌雄各半,体重(300±30)g,随机分为益气活血方组、缺血再灌注组、假手术组,每组10只。结扎冠状动脉左前降支后30min,再松开结扎线120min,以制备急性心肌梗死(AMI)缺血再灌注损伤模型。实验结束后,迅速取出心脏,生理盐水冲洗后,10%甲醛固定24h。常规石蜡包埋,于心肌梗死区中部沿左室轴线每隔1mm连续切取数张4μm厚的切片,分别作苏木精-伊红染色,进行心肌组织病理形态学检查。结果益气活血方能减轻缺血再灌注时心肌组织及细胞超微结构的形态学损伤。益气活血方组细胞核结构似假手术组,核周间隙仍有轻度肿胀,线粒体超微结构与假手术组相仿。结论益气活血方对心肌缺血再灌注损伤具有保护作用。     

气活血法对大鼠心肌缺血再灌注损伤保护作用的实验研究

目的 探讨按益气活血法制定的益气活血方对心肌缺血再灌注损伤的保护作用.方法 清洁级健康SD大鼠30只,雌雄各半,体重(300±30)g,随机分为益气活血方组、缺血再灌注组、假手术组,每组10只.结扎冠状动脉左前降支后30 min,再松开结扎线120 min,以制备急性心肌梗死(AMI)缺血再灌注损伤模型.实验结束后,迅速取出心脏,生理盐水冲洗后,10%甲醛固定24h.常规石蜡包埋,于心肌梗死区中部沿左室轴线每隔1 mm连续切取数张4 μm厚的切片,分别作苏木精-伊红染色,进行心肌组织病理形态学检查.结果 益气活血方能减轻缺血再灌注时心肌组织及细胞超微结构的形态学损伤.益气活血方组细胞核结构似假手术组,核周间隙仍有轻度肿胀,线粒体超微结构与假手术组相仿.结论 益气活血方对心肌缺血再灌注损伤具有保护作用.     

含抑肽酶灌注液减轻缺血再灌注心肌的损伤

目的　观察抑肽酶等药物对缺血再灌注离体兔心的影响。方法　 2 4只家兔随机分为两组 :对照组 (B组 )将离体心脏置于 L angendorfl装置 ,经主动脉逆行灌注克氏液 ,灌注 30 min后 ,用 Thomas灌注停跳 40 min,最后再恢复灌注 30 min。用药组 (A组 )克氏液中加入抑肽酶及山莨菪碱。缺血前及再灌注期记录左心室功能及冠状动脉血管阻力 ,并行心肌超微结构观察。结果　再灌注后 30 min,A组左心室功能明显高于 B组 (P<0 .0 5 ) ;收集的灌注液中肌酸磷酸激酶 (CK)及乳酸脱氢酶 (L DH)较 B组明显减少 ;超微结构改善也优于 B组。结论　抑肽酶对缺血再灌注心肌功能有明显保护作用     

兔心房室结缺血再灌注损伤的超微结构变化及BCL-2表达

目的用健康兔做在体心房室结缺血再灌注损伤模型,观察房室结缺血再灌注损伤的超微结构变化及BCL-2基因蛋白表达。方法健康兔30只,随机分为3组,A组(假手术组)n=10,B组(缺血30min,再灌注30min)n=10,C组(缺血30min,再灌注240min)n=10。结果A组血清天冬酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、肌酸肌酶(CK)未升高,免疫组化检测房室结BCL-2基因蛋白未见表达,超微结构无变化。B、C组AST、LDH、CK及BCL-2基因蛋白表达逐渐升高,超微结构中细胞水肿逐渐明显,线粒体肿胀、嵴断裂逐渐明显,肌丝逐渐收缩,细胞核染色质集块边聚明显。结论心房室结缺血再灌注损伤随再灌注时间延长变化明显。     

磷酸肌酸对大鼠缺血再灌注后心肌损伤的影响

目的 观察磷酸肌酸对大鼠缺血再灌注后心肌损伤的影响.方法 60只雄性SD大鼠随机分为假手术组、模型组、磷酸肌酸组.结扎大鼠左前降支冠状动脉使心肌缺血,30 min后恢复血流并持续120 min,复制缺血再灌注损伤模型.磷酸肌酸组分别于缺血再灌注前30 min经右颈内静脉注射磷酸肌酸3 mg/kg,模型组及假手术组给予等量的生理盐水.测定血清乳酸脱氢酶(LDH)、磷酸肌酸激酶(CK)及心肌组织丙二醛(MDA)和超氧化物歧化酶(SOD)的含量并观察心肌超微结构的变化.结果 磷酸肌酸组与模型组比较,血清LDH、CK值降低,心肌组织MDA值减小,SOD值升高.光镜及电镜下心肌细胞变性坏死程度及心肌细胞超微结构形态改变显著减轻.结论 磷酸肌酸对大鼠心肌缺血再灌注损伤均有保护作用.     

犬肺缺血预处理对体外循环心肌的影响

目的探讨肺缺血预处理对体外循环心肌的保护作用及机制。方法12只健康杂种犬,体重12～15kg,随机分为实验组和对照组,每组6只。对照组为单纯体外循环组;实验组为缺血预处理组,在主动脉阻断前行左肺门阻断5min,再灌注5min,重复一次,然后同对照组行体外循环,两组体外循环均持续1h。于体外循环前、再灌注120min后采集心肌标本,测定心肌含水量、MDA、SOD活性及病理改变。结果体外循环后心肌含水量和MDA实验组低于对照组;心肌SOD活性实验组高于对照组;实验组心肌标本炎症水肿程度明显较对照组轻。结论犬肺缺血预处理对体外循环心肌缺血再灌注损伤有保护作用,其机制可能是减轻了心肌缺血再灌注损伤。     

Effects of reperfusion on myocardial wall thickness, oxidative phosphorylation, and Ca2+ metabolism following total and partial myocardial ischemia

Coronary artery reperfusion following acute myocardial ischemia may salvage ischemic jeopardized cells. We studied the effects of early brief reperfusion on totally ischemic and on partially ischemic myocardium of open-chest pigs. In 10 animals, coronary flow was reduced to 0% for 30 minutes and was followed by 10 minutes reperfusion (group A). In another 10 animals, coronary flow was reduced to 25% of the baseline value for 30 minutes followed by 10 minutes of reperfusion (group B). In another eight animals coronary flow was reduced to 25% of the baseline value for 60 minutes and followed by 10 minutes of reperfusion (group C). Results showed that a brief 10-minute period of reperfusion of ischemic myocardium after total occlusion caused abnormal diastolic wall thickening with only partial return of systolic wall thickening. However, reperfusion of ischemic myocardium after partial occlusion, whether 30 or 60 minutes, caused little diastolic wall thickening and a partial return of systolic thickening. A marked elevation of myocardial Ca2+, a decrease in mitochondrial adenosine triphosphate (ATP) production and cellular ATP concentration, and a reduction in the rate of Ca2+ uptake by sarcoplasmic reticulum vesicles occurred in the totally ischemic myocardium but not in the partially ischemic myocardium. These results demonstrate that reperfusion of ischemic myocardium after 1 hour of coronary flow reduction to 25% of baseline is less damaging than reperfusion after a 30-minute total coronary occlusion, and suggest that preexisting states affecting coronary flow need to be evaluated in assessing the outcome of reperfusion.     

Hyaluronidase does not prevent deterioration of vascular functional integrity during reperfusion after no-flow ischemia in isolated rabbit hearts

Effects of hyaluronidase on myocardial water content and distribution, and on coronary vascular hemodynamics and endothelial cell transport function were assessed in isolated rabbit hearts during 3.5 hours of reperfusion after 30 minutes of global, no-flow ischemia. In nonischemic control hearts, perfusion pressure, left ventricular end-diastolic pressure, maximum +dP/dt, and intravascular clearance of radiolabeled albumin remained constant during 5 hours of continuous perfusion, while the mean-transit time and vascular into extravascular space clearance of radiolabeled albumin increased 1.5X and 2.5X baseline, respectively. During reperfusion after 30 minutes of no flow, perfusion pressure increased 53% and interstitial fluid volume increased 2-fold, while left ventricular end-diastolic pressure and maximum +dP/dt returned to control levels. The rate of intravascular clearance of radiolabeled albumin decreased 38%, and the mean-transit time and vascular-into-extravascular space clearance of albumin increased approximately 3X and 5X baseline, respectively. Hyaluronidase blocked the ischemia-reperfusion-induced increases in total water content and in interstitial fluid volume and reduced the increases in perfusion pressure and mean-transit time of radiolabeled albumin by 40% and 45%, respectively, but did not prevent the increase in albumin vascular-into-extravascular space clearance and the decrease in albumin clearance from the coronary vasculature. These findings indicate that hyaluronidase does not prevent ischemia-reperfusion-induced increases in albumin permeation of the coronary vasculature, and suggest that its protective effect on ischemic myocardium is mediated, instead, by reducing interstitial edema and vascular resistance.     

The experimental study of the coronary reperfusion in the acute myocardial ischemia: the feasibility of the myocardial salvage

In order to know the feasibility of coronary reperfusion by thrombolysis or aorto-coronary bypass graft in the early stages of the acute myocardial infarction, we studied the effect of the coronary artery reperfusion to acutely ischemic myocardium induced by the coronary artery occlusion in ninety-five anesthetized open-chest dogs. The major factors determining the extent of the myocardial salvage by the reperfusion were the duration of the occlusion time and the degree of the reperfusion injury. These two determinants were analysed by coronary circulation, the regional myocardial function, the mitochondrial metabolism, mitochondrial Ca and Mg contents, and morphological findings of the myocardium by electron-microscopy. The regional myocardial contractility (% systolic shortening) and the mitochondrial metabolism (oxidative phosphorylation) were significantly damaged by the reperfusion more in 60 minute occlusion than in 30 minute occlusion, although the coronary circulation (coronary blood flow, regional myocardial blood flow and coronary vascular resistance) and myocardial gas contents (PO2, PCO2 and pH) in the ischemic myocardium induced by less than 60 minute occlusion were almost recovered to the pre-occluded level by 60 minutes after reperfusion. By 120 minute reperfusion, the ischemic damage calculated from mitochondrial Ca and Mg contents (MC index: 1-[Mg/Ca] ischemia/[Mg/Ca] non-ischemia) was not changed in 30 minute occlusion but was significantly deteriorated in 60 minute occlusion. Therefore, coronary reperfusion must be started within 60 minutes or less after occlusion. A supplementary way to protect the myocardium from ischemia is needed as soon as possible before reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Protective effects of ginsenosides in myocardial ischemia and reperfusion injury

To verify whether ginsenosides will attenuate the myocardial ischemia and reperfusion injury, the left anterior descending coronary artery (LAD) was snared for 2 hours in 23 dogs and then the ischemic myocardium was reperfused. 45 minutes after ischemia, the animals were randomly divided into a ginsenosides group (n = 11, receiving a slow IV bolus of ginsenosides 10 mg/kg and then a continuous infusion of 80 micrograms/kg/min) and a saline solution group (n = 12 receiving equal amount of glucose in saline). The treatment was started 45 minutes after coronary occlusion and stopped one hour after reperfusion. 24 hours later, the dogs were killed and the extent of myocardial necrosis was determined histologically. The LVEDP, arterial pressure and heart rate were markedly lower in the ginsenosides group. Electrocardiographic findings of myocardial ischemia were significantly improved in the ginsenosides group. 8 controls developed malignant arrhythmia after reperfusion, but none in ginsenosides group. The myocardial ultrastructure can be protected by ginsenosides during the period of ischemia and reperfusion. The infarct size in saline group was 22.7 +/- 3.2% while in the ginsenosides group it was 5.2 +/- 1.3% (P less than 0.05). These results show that ginsenosides can protect the ischemic myocardium and reperfusion injury of myocardium.     

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.     

经心内膜注射血管内皮生长因子基因治疗猪心肌缺血模型的远期效果观察

目的:探讨经心内膜心肌内直接注射血管内皮生长因子(vascular endothelial growth factor,VEGF)基因治疗猪心肌缺血模型后,远期心功能以及局部超微结构的变化。方法:将30只实验用小香猪均分为对照组(n=15)和治疗组(n=15)。以冠状动脉内球囊建立心肌缺血模型后,通过NOGA系统经心内膜将空质粒和pIRES2-EGFP-hVEGF165质粒分别直接注射至对照组和治疗组猪的缺血部位心肌内。在注射前及注射后1年,应用超声检测M型局部室壁的运动幅度和背向散射积分的心动周期变异(cardiac cycle variation of integrated backscatter,CVIB)和左心室射血分数(Left ventricular ejection fraction,LVEF)。1年后处死动物,通过检测Ⅷ因子的SABC染色法观察心肌组织中毛细血管生成的情况,并以透射电子显微镜观察局部超微结构的变化。结果:与对照组相比,治疗组术后1年时,M型局部室壁的运动幅度和CVIB、LVEF均显著增加(P0.05)。检测Ⅷ因子的SABC染色法显示,对照组心肌内毛细血管数目为(13±5)个/HP;而治疗组为(38±5)个/HP(P0.01)。透射电子显微镜观察发现,对照组梗死区残存心肌存在严重的心肌细胞萎缩,缺血区心肌肌丝出现不同程度纵向断裂,线粒体排列紊乱,时有肿胀、变性;而治疗组残存心肌仅轻度萎缩,缺血区心肌的结构较为正常。结论:猪心肌缺血模型经心内膜直接注射pIRES2-EGFP-hVEGF165基因后,远期可增加缺血心肌部位的血管新生,促进局部心肌细胞结构的恢复,从而改善心功能。     

缺血后处理减轻心肌线粒体损伤对缝隙连接蛋白43的影响

目的观察缺血后处理对线粒体缝隙连接蛋白43(Cx43)的影响以及心肌保护的可能机制。方法健康新西兰大白兔64只.建立心肌缺血再灌注模型,随机分为4组,假手术组、缺血再灌注组、缺血预处理组、缺血后处理组,每组16只。检测各组心肌梗死面积,透射电镜观察心肌细胞的超微结构,荧光法检测线粒体膜电位,比色法检测线粒体Ca~(2+)和丙二醛浓度及超氧化物歧化酶(SOD)活性,Western blot法检测Cx43含量。结果与缺血再灌注组比较,缺血后处理组和缺血预处理组兔心肌梗死面积明显减少,心肌线粒体形态结构改变明显减轻,跨膜电位、SOD活性、线粒体Cx43明显升高,Ca~(2+)、丙二醛浓度明显降低(P<0.05,P<0.01)。与假手术组比较,缺血再灌注组兔线粒体Cx43明显下调(P<0.05)。结论缺血后处理保护心肌及线粒体可能与提高线粒体跨膜电位、降低线粒体氧自由基水平和减轻线粒体Ca~(2-)超载有关,其机制可能与提高线粒体Cx43表达有关。     

Proteomic Mechanism of Myocardial Angiogenesis Augmented by Remote Ischemic Training of Skeletal Muscle in Rabbit

Aims: This study was designed to evaluate the proteomic mechanism of myocardial angiogenesis augmented by a remote ischemic training (RIT) of skeletal muscle in a controlled myocardial ischemia model. Methods: The rabbits were grouped by RIT, myocardial ischemia without RIT (MI), and sham‐operation (Sham). Controlled myocardial ischemia was modeled by a balloon constrictor implanted on their left ventricular branch (LVB) in a New Zealand rabbit. RIT was induced by four cycles of 10‐minute ischemia followed by 10 minutes of reperfusion using tourniquets on the hind limbs of the myocardial ischemia models for 4 weeks. The myocardial samples were subjected to two dimensional electrophoresis and MALDI TOF for protein identification. The angiogenesis was documented by using microspheres to measure the relative regional blood flow, immunohistochemistry to assess capillary density (Factor VIII), and Western blotting to measure the vascular endothelial growth factor (VEGF) levels. Results: Thirty‐eight differentially expressed protein spots between RIT and MI were separated by two‐dimensional gel electrophoresis, and of those, 22 proteins were identified by mass spectrometry. The regional blood flow, capillary density and VEGF in RIT were 35%, 49% and 28% higher than MI (p < 0.01). The increase of regional blood flow and capillary density were highly correlated with VEGF (r= 0.74 and r= 0.67, respectively; p < 0.01). Both RIT and MI groups exhibited stronger angiogenesis than sham treatment (p < 0.01). Conclusions: Augmentation of angiogenesis in ischemic myocardium by RIT has identical identified proteomic findings with differentially expressed proteins.     

Normothermic ischemic cardiac arrest of the isolated working rat heart. Effects of time and reperfusion on myocardial ultrastructure, mitochondrial oxidative function, and mechanical recovery

The ischemic state of the myocardium of the isolated working rat heart after induction of normothermic ischemic cardiac arrest was assessed by the interrelationship among changes in myocardial ultrastructure, mitochondrial oxidative phosphorylation, and tissue high energy phosphate contents. At all time intervals (10-40 minutes) studied, the ultrastructural changes were more severe in the subendocardium than in the subepicardium. After 25-40 minutes of normothermic ischemic cardiac arrest, the mitochondrial oxygen uptake (state 3) became increasingly depressed, particularly in mitochondria isolated from the subendocardium. Mitochondrial oxidative function, as measured in vitro, did not correlate well with mitochondrial ultrastructural damage. In addition, the effects of coronary reperfusion on the ability of the ischemic heart to recover in terms of ultrastructure, mechanical, and metabolic function were evaluated. Hearts subjected to 10-40 minutes of normothermic ischemic cardiac arrest showed almost complete ultrastructural recovery of the subepicardium upon reperfusion; regression of ultrastructural changes occurred to a lesser extent in the subendocardium. Reperfusion for 30 minutes did not alleviate the depression in mitochondrial oxidative function, while tissue ATP levels did not return to control, preischemic levels. After 20 minutes of normothermic ischemic cardiac arrest, the mechanical performance of the working heart during reperfusion was significantly depressed, compared with pre-ischemic control values. Normal ultrastructure of the subendocardium always accompanied mechanical recovery, while improvement of mitochondrial oxidative function was not essential.