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运动后复氧对心脏结构功能的影响 被引量:22

Effect On The Structure Of Heart During Re-oxygen Process
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摘要 力竭性运动引起心肌组织相对缺氧缺血引发心肌结构功能改变,在复氧期其变化持续加重。表现在心肌线粒体出现肿胀、嵴断裂、内外膜崩解破裂、肌原纤维紊乱、横小管及肌质网扩张、肌小节紊乱、断裂、解聚、粗肌丝减少、肌原纤维间间隙增大、细胞膜及核膜结构不清等现象,以及心肌收缩舒张功能降低,心肌细胞内钠钙聚集、ATP减少、酸性物增加,胞外钾聚集,自由基生成增多等功能改变。其生理机制主要与心肌能量代谢改变及自由基生成等因素有关。 Hypoxia and ischemic of myocardium due to exhausted exercise could result in the change of structure and function of cardiac muscles, and the change will aggravate persistently during the re-oxygen process. Under microscopy, the change of the subcellular structure include:1) mitochondria swell company with cristae break and disintegration of inner and outer membrane; 2)the gap between muscle fibrils become broaden and the alignment of muscle fibril turn to disordered; 3)the T tube and sarcoplasmic reticulum of cardiac muscle cells become broaden; 4)derangement, collapse and depolymerize of sarcomere company with reduction of myosin filament. The contract and diastolic function of cardiac muscles also decrease accompany several physiological changes inner myocardium cells such as aggregation of calcium and sodium , increase of acid metabolite and decrease of ATP, and outer myocardium cells such as aggregation of potassium and increase of free radicals, etc. The mechanism of these changes may be related to the change of energy metabolism of myocardium and the formation of free radical.
作者 苏全生
机构地区 成都体育学院
出处 《成都体育学院学报》 CSSCI 北大核心 2004年第3期61-64,共4页 Journal of Chengdu Sport University
关键词 运动性疲劳 心脏 自由基 运动性缺血再灌注损伤 Sports fatigue heart free radical exercise ischemical reperfusion injury
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