中文摘要：

目的：观察大鼠心室颤动过程中心肌线粒体能量代谢障碍的病理生理变化，进一步探讨心肺复苏改善室颤心肌线粒体能量代谢障碍的保护作用。方法：经右心室内膜交流电致颤建立大鼠心跳骤停模型，随机分组：（1）心肺复苏组，10min心室颤动后，给予5min的机械胸外按压和同步通气；（2）单纯心室颤动组，持续15min的心室颤动．不予心肺复苏；（3）正常对照组，15min后，立即开胸取出大鼠心脏，抽提心肌线粒体检测线粒体呼吸功能，取心肌组织送检透射电镜以及检测糖原含量。结果：心肺复苏组线粒体Ⅲ态呼吸和呼吸控制率均小于正常对照组（P〈0．05），但仍高于单纯心室颤动组（P〈0．05），心肺复苏组和心室颤动组心肌糖原含量均小于正常对照组（P〈0．05），其中心肺复苏组糖原含量低于心室颤动组（P〈0．05）。电镜下心肺复苏组心肌线粒体损伤明显较心室颤动组轻。结论：室颤引起心肌线粒体呼吸功能损伤；心肺复苏通过减轻线粒体呼吸功能损伤，有效地减轻能量代谢障碍。

英文摘要：

Objective：To investigate the pathophysiological change of myocardial mitochondrial energy metabolism during ventrlcular fibrillation （VF） in a rat model, and to observe the effectiveness of cardiopulmonary resuscitation （CPR） at ameliorating mitochondrial metabolic disorder. Methods： VF was electrically induced via alternating current delivered to the right ventricular endocardium. Animals were randomized into three groups： 1 ） CPR group; 2） VF Group; and 3） control group. The rat heart was quickly removed at the predetermined time point of 15 mins for the measurements of mitochondrial function, mitochondrial uhrastructure and myocardial glycogen. Results： The levels of State 3 and respiratory control rate in CPR group were significantly less than control group （P〈0.05）, whereas greater than those in VF group （P〈0.05）. The glycogen content in both CPR group and VF group were significantly less than that of control group （P〈0.05）. The glycogen level in CPR group were significantly decreased compared with VF group （P〈0.05）. The mitochondrial uhrastructural abnormalities in CPR group were less severe than VF group. Conclusions： VF provokes significant impairment of myocardial mitochondrial respiratory function in a rat model of cardiac arrest. We further observe that CPR can ameliorate the energy metabolic disorder via protecting mitochondrial function.