心肺复苏对心脏骤停大鼠脑线粒体功能的保护作用

Protective Effect of Cardiopulmonary Resuscitation on Brain Mitochondrial Function in a Rat Model of Cardiac Arrest

【目的】探讨心肺复苏对心脏骤停大鼠脑神经元线粒体功能的保护作用。【方法】建立大鼠室颤法心脏骤停模型,缺血组心跳停止15 min,不行心肺复苏,复苏组心跳停止10 min,行5 min心肺复苏。15 min末处死动物,分离提取海马脑组织线粒体,用Clark氧电极法检测线粒体呼吸功能,线粒体内、外膜试剂盒测定线粒体膜完整性,电镜观察线粒体超微结构。【结果】心脏骤停后,缺血组和复苏组的线粒体外膜完整率、内膜膜电位、呼吸控制率均较假手术组明显降低(P<0.01),复苏组结果高于缺血组(P<0.01),形态学比较各组间无显著差异。【结论】心脏骤停早期,神经元线粒体损伤以功能性为主,形态学改变不明显,心肺复苏可改善缺血神经元的线粒体功能,减轻脑线粒体损伤。

[Objective] To investigate the protective effect of cardiopulmonary resuscitation （CPR） on brain mitochondrial function in a rat model of cardiac arrest. [ Methods ] Cardiac arrest rat model was established by electrical induced ventricular fibrillation. The SD rats were randomly divided into： ischemia group, in which 15 min of cardiac arrest was induced without CPR; CPR group, in which 10 min of cardiac arrest was performed followed by 5 min of CPR; and sham control group. The rats were sacrificed at the end of 15 min and hippocampal mitochondrion was isolated and extracted. Clark oxygen electrode was used to measure mitochondrial respiratory function. Mitochondrial membrane kits were used to examine the integrity of mitochondrion. Mitochondrial ultra structure was observed with transmission electron microscope. [ Results ] After cardiac arrest, the integrity of mitochondrial outer membrane, mitochondrial membrane potential and respiratory control rate in ischemia group and CPR group were significantly decreased than those in sham operation group （P 〈 0.01 ）. The result of CPR group was higher than that of ischemia group （P 〈 0.01 ）. There was no morphological difference between each group. [ Conclusion ] In the early stage of cardiac arrest, the brain mitochondrial impairment mainly manifested as functional damage rather than morphological injury. CPR could improve mitochondrial function and alleviate injury of isehemic neurons.