间歇性低氧防止缺血再灌注损伤引起的线粒体结构损伤和mtDNA片段缺失(英文)  

Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury 

作　　者：钟宁[1] 张翼 朱海峰 周兆年[1] 

机构地区：[1]中国科学院上海生理研究所低氧心血管生理实验室,上海200031

出　　处：《生理学报》2000年第5期375-380,共6页Acta Physiologica Sinica

基　　金：SupportedbytheShanghaiInstitutesforBiologicalSciences

摘　　要：本文用离体Langendorff灌流大鼠心脏造成急性心肌缺血 /再灌注损伤模型 ,观察间歇性低氧暴露保护心肌线粒体的作用。以聚合酶链式反应 (PCR)方法和电子显微镜技术 ,观察线粒体DNA (mtDNA4 834 )片段缺失和超微结构的变化。大鼠暴露于模拟海拔 5 0 0 0米低氧环境 (6h/d ,2 8d)明显降低mtDNA4 834 缺失的发生率 (2 8 5 7% ,vs常氧对照组 87 5 %P <0 0 5 ) ;而且能够明显减轻因缺血 /再灌注引起的心肌线粒体肿胀、线粒体嵴断裂、消失 ;较好地维持了线粒体的正常结构和形态。结果表明 ,间歇性低氧暴露能有效防止缺血 /再灌注引起的心肌线粒体损伤和mtDNA的片段缺失 ,此作用可能是间歇性低氧心肌保护作用的机制之一。WT5”BZ] In the present study, polymerase chain reaction (PCR) was conducted to determine mtDNA 4834 deletion, and myocardial ultrastructure was visualized by electron microscope to see whether intermittent hypoxia (high altitude) adaptation exerts some action on mitochondria against ischemia/reperfusion injury. Myocardial ischemia/reperfusion in isolated perfused rat hearts induced severe damage to the ultrastructure of myocardial mitochondria and mtDNA 4834 deletion down to 87 5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5?000 m; 6 h/d for 28 d), the myocardial structure was well reserved and mtDNA 4834 deletion dropped to 28 57% of control ( P <0 05). It is suggested that intermittent hypoxia adaptation prevents mtDNA deletion, and preserves normal structure of mitochondria, which would be beneficial to the maintenance of normal mitochondrial function, and increases tolerance of myocardium against ischemia/reperfusion injury.

关 键 词：MTDNA 缺血/再灌注损伤 间歇性低氧 超微结构 

分 类 号：R542.205[医药卫生—心血管疾病] Q494[医药卫生—内科学]