目的研究心肺复苏后大鼠脑细胞线粒体呼吸功能及能量代谢的改变。方法采用窒息合并冰氯化钾停跳液致大鼠心跳骤停5min后开始心肺复苏的动物模型,SD大鼠48只,随机分为6组:对照组(假手术组)、复苏后3、12、24、48和72h组(每组8只)。各组取脑组织测定线粒体呼吸Ⅲ、Ⅳ态及呼吸控制率(RCR),磷氧比(P/O);应用高效液相及紫外检测法测定脑细胞ATP、ADP和AMP含量及能荷值。结果心肺复苏后大鼠脑细胞线粒体功能明显受损,线粒体呼吸Ⅲ态速率下降,线粒体呼吸Ⅳ态速率升高,线粒体呼吸控制率(RCR)和P/O明显下降;随着复苏成功后时间的延长,脑细胞线粒体呼吸控制率(RCR)和P/O持续下降,其中,24h有所恢复,48h再次下降;心肺复苏后的脑细胞ATP含量明显下降,ADP和AMP相对增加。结论心肺复苏后大鼠脑细胞线粒体呼吸功能明显下降,能量代谢障碍。
[Objective] To observe changes in mitochondria respiratory function and energy metabolism of brain cells in mrs after cardiopulmonary resuscitation(CPR). [Methods] Cardiac arrest was induced by asphyxiation and ice-cold 0.5 M KC1 and resuscitation was started in five minutes after arrest. Fourty-eight Sprague Dawley rats were divided into 6 groups randomly: sham (control group); after cardiopulmonary resuscitation rats were allowed to reperfuse spontaneously for 3 hours, 12 hours, 24 hours 48 hours and 72 hours (n=8, per group). Clark oxygen electrode was used to measure the change in brain mitochondrial respiratory state In, 1V and respiratory control rate(RCR), the phosphor ratio (P/O) after Cardiopulmonary Resuscitation, in order to evaluate mitochondrial respiratory function (MRF); The levels of ATP (adenosine triphosphate), ADP (adenosine diphosphate), and AMP (adenosine monophosphate) in brain tissue were determinated by high performance liquid chromatography with electrochemical and ultraviolet detection. Using the Neural Deficiet Scores (NDS) evaluate the nerve functions of rats. Camitine(100 mg/kg) was given intraperitoneally after Restoration of spontaneous circulation (ROSC). [Results] Mitochondria respiratory function of brain ceils were damaged after CA/CPR, as indicated by decrease of respiratory control rate(RCR) and the phosphor ratio (P/O) (P〈0.05, 0.01). On the other hand, the level of ATP was significandy decreased after resuscitation (P〈0.05). [Conclusion] The MRF, content of ATP, and the eneraKe burden is damaged significantly by CA/CPR.