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目的 探讨慢性缺血导致的冬眠心肌(hibernating myocardium,HM)的线粒体形态和功能的改变,拟阐明线粒体相关的心肌冬眠的机制.方法 通过外科开胸置入Ameriod缩窄环的方法建立巴马猪的HM模型,通过多巴酚丁胺负荷超声心动图(dobutamine stress echocardiography,DSE)验证,观察对心功能、室壁运动、线粒体功能的改变.结果 HM模型手术成功率为67％,与假手术组相比,模型组有明显室壁运动异常,DSE示节段性的双相运动反应,室壁增厚率降低,射血分数降低.HM的HE染色和电镜观察分别表现出心肌纤维和线粒体在形态、排列、结构上的异常.模型组的线粒体呼吸链酶复合物Ⅰ、Ⅱ、Ⅲ的活性较假手术组降低,(分别为268.75±18.75％vs 118.75±11.97％;217.50±14.93％ vs 155.00±2.89％;245.83±18.48％ vs 169.23±15.70％),p值均小于0.05,差异有统计学意义.线粒体呼吸链酶复合物V即ATP合成酶的活性降低了32.51％,组间差异有统计学意义.结论 慢性缺血导致的心肌冬眠伴随着线粒体功能的减低,可能是HM在缺血中保持其存活的手段.“,”Objective To observe the morphological and functional changes of mitochondria in ischemia caused myocardial hibernation,and the underlying mechanism.Method Establish swine model of hibernating myocardium(HM) through thoracotomy approach by placing Ameroid constrictor,and verify by dobutamine stress echocardiography(DSE),observe the changes in cardiac function,wall motion,and activity of mitochondria respiratory enzyme complexes.Result Compared with the control group,model group had abnormal ventricular wall motion,and ejection fraction were reduced,ventricular wall thickening rate was lower in model group,during DSE the HM showed biphasic responses.HE staining and electron microscope showed changes in myocardial fibers and mitochondria in the form,arrangement,structures.The activity of complex Ⅰ,Ⅱ,Ⅲ were reduced in model group (268.75±18.75％ vs 118.75±11.97％,217.50±14.93％ vs 155.00±2.89％,245.83±18.48％ vs 169.23±15.70％) p ＜0.05,the difference was statistically significant.The complex V activity was reduced by 32.51％,the difference between two groups was statistically significant.Conclusion There were mitochondria dysfunction in chronic ischemia caused HM,and it may be the mechanism of HM to keep its viability during the ischemia.