摘要
目的:探讨缺氧大鼠心肌线粒体呼吸功能和心肌能量代谢的变化。方法:通过Clark氧电极法和生化方法测定线粒体功能和FoF1-ATP酶活力,运用高效液相色谱技术(HPLC)测定心肌组织ATP含量。结果:急性缺氧大鼠心肌线粒体呼吸功能,FoF1-ATP酶活力以及1-苯胺基,8-萘磺酸镁(ANS)相对荧光强度明显降低(P<0.01),表明:FoF1-ATP酶构象发生改变。心肌组织ATP含量明显减少(P<0.01)。慢性缺氧上述指标不同程度有所恢复,但仍明显低于平原水平。经相关分析表明:ATP含量与线粒体呼吸控制率(RCR),FoF1-ATP酶活力及PaO2呈明显正相关(P<0.01)。结论:急性缺氧动物心肌能量代谢障碍可能与心肌线粒体呼吸功能降低,FoF1-ATP酶活力降低有关系。慢性缺氧后能量代谢的改善,可能是缺氧适应的机理之一。
Objective: To determine the changes of myocardial energy metabolism in hypoxic rats. Method: 30 adult Wistar rats were equally devided into three groups: 1)normal control group; 2)actuhypoxic group; 3)chronichypoxic group. The changes of respiratory function, activity of FoF1ATPase and ANS fluroescense intensity in myocardial mitochondria were observed with clark oxygen electrode and tiochemical method and the content of ATP in myocardial tissue measured with high performance liquid chromatography (HPLC). Results: 1)The respiratory function, FoF1ATPase activity and ANS flurosecense intensity were significantly decreased in acutehypoxic. Though the above parameters were increased in chronichypoxic group as compared with thore in the acutehypoxic group, they remained lower than those in the control. 2)ATP content was positively correlated to PCR, FoF1ATPase activity and PaO2. Conclusion: The failure of myocardial energy metabolism in acutehypoxic rats may be due to the decrease of mitochondrial respiratory. function and ATP production. The improvement of energy metabolism in chronichypoxic rats in one of the mechanisms for hypoxic adjustment.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1997年第3期240-242,共3页
Journal of Third Military Medical University
关键词
缺氧
线粒体
ATP
心肌
呼吸功能
hypoxia
mitochondrial function
FoF1ATPase
ATP content
rat