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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,10 min心室颤动后,给予5 min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,15 min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。
OBJECTIVE: To observe the pathophysiological changes of myocardial mitochondrial energy metabolism during the process of ventricular fibrillation, and to further explore the protective effect of CPR on mitochondrial energy metabolism in ventricular fibrillation. Methods: A rat model of cardiac arrest was established by right ventricular fibrillation. The rats were randomly divided into the following groups: (1) cardiopulmonary resuscitation (CPR) group, mechanical chest compression and synchronized ventilation for 5 min after 10 min ventricular fibrillation; (2) Ventricular fibrillation for 15 min, no cardiopulmonary resuscitation; (3) Normal control group, immediately after thoracotomy, rat heart was removed by thoracotomy. Mitochondria were extracted for myocardial mitochondrial respiratory function, and myocardial tissue was taken for transmission electron microscopy As well as detecting glycogen content. Results: The levels of mitochondrial third-state respiration and respiratory control in CPR group were significantly lower than those in normal control group (P <0.05), but were still higher than those in simple ventricular fibrillation group (P <0.05). The levels of cardiac glycogen in CPR group and ventricular fibrillation group (P <0.05), and the content of glycogen in cardiopulmonary resuscitation group was lower than that in ventricular fibrillation group (P <0.05). The myocardial mitochondrial damage in cardiopulmonary resuscitation group under electron microscope was obviously lighter than that in the ventricular fibrillation group. CONCLUSION: Ventricular fibrillation causes mitochondrial respiratory dysfunction; cardiopulmonary resuscitation (CPR) mitigates energy metabolism disorders by alleviating mitochondrial respiratory dysfunction.