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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

钟宁, 张翼, 朱海峰, 周兆年

中科院上海生理研究所低氧心血管生理实验室.上海 200031

摘要

大鼠暴露于模拟海拔5 000米低氧环境(6h/d,28d)明显降低mtDNA~(4834)缺失的发生率(28.57%,vs常氧对照组87.5%,P<0.05);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。

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

Zhong Ning, Zhang Yi, Zhu Haifeng, Zhou Zhaonian

Physiological Laboratory of Hypoxia,Shanghai Institute of Physiology,Chinese Academy of Sciences.Shanghai 200031

Abstract

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.

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引用本文：

钟宁, 张翼, 朱海峰, 周兆年. 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[J]. 生理学报 2000; 52 (5): 375-380.

Zhong Ning, Zhang Yi, Zhu Haifeng, Zhou Zhaonian. Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury. Acta Physiol Sin 2000; 52 (5): 375-380 (in Chinese with English abstract).