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为探讨缺氧缺血对脑细胞线粒体氧化磷酸化功能的影响及苯巴比安干预效果，本实验将7日龄Wistar大风制成缺氧缺血模型，测定脑细胞线粒体呼吸控制比（RCR），最大呼吸连度（MRR）、ATP合成量，并同时设正常对照组，苯巴比妥干预治疗组。结果显示：缺氧缺血红线粒体RCR、MRR、ATP今成量明显低于正常对照组；干预治疗后，RCR、MRR、ATP合成量较缺氧缺血组明显升高。证实，缺氧缺血可损伤线粒体氧化磷酸化功能，而苯巴比妥对线粒体功能恢复有促进作用。
In order to investigate the effect of hypoxia-ischemia on mitochondrial oxidative phosphorylation in brain cells and the effect of phenobarbital intervention, a 7-day-old Wistar gale model was made to establish hypoxia-ischemia model to measure mitochondrial respiratory control ratio (RCR) , Maximum respiratory connection (MRR), ATP synthesis, and at the same time set the normal control group, phenobarbital intervention group. The results showed that the present dose of RCR, MRR and ATP of mitochondria of hypoxia and ischemia were significantly lower than those of normal control group. After intervention, the synthesis of RCR, MRR and ATP was significantly higher than that of hypoxia-ischemia group. Confirmed that hypoxia and ischemia can damage mitochondrial oxidative phosphorylation function, and phenobarbital on mitochondrial function recovery.