Zhong N, Zhang Y, Zhu H F, Zhou Z N
Physiological Laboratory of Hypoxia, Shanghai Institute of Physiology, Chinese Academy of Sciences, Shanghai 200031, China.
Sheng Li Xue Bao. 2000 Oct;52(5):375-80.
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 mtDNA4834 deletion down to 87.5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5000 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.
在本研究中，采用聚合酶链反应（PCR）检测线粒体DNA（4834）缺失情况，并用电子显微镜观察心肌超微结构，以探究间歇性低氧（高原环境）适应是否对线粒体抵抗缺血/再灌注损伤有一定作用。在离体灌注大鼠心脏中，心肌缺血/再灌注对心肌线粒体超微结构造成严重损伤，线粒体DNA4834缺失率降至常氧大鼠的87.5%。大鼠暴露于间歇性低氧环境（海拔5000米；每天6小时，共28天）后，心肌结构得到良好保留，线粒体DNA（4834）缺失率降至对照组的28.57%（P<0.05）。这表明间歇性低氧适应可防止线粒体DNA缺失，保留线粒体正常结构，这有利于维持线粒体正常功能，并增加心肌对缺血/再灌注损伤的耐受性。
