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目的：探讨脑缺血与再灌流后线粒体呼吸功能变化以及与脑水肿的关系。方法：采用Ｃｌａｒｋ氧电极法测定脑缺血及再灌流后脑细胞线粒体呼吸Ⅲ、Ⅳ态及呼吸控制率（ＲＣＲ）；采用烘干法按Ｅｌｉｓ公式计算脑含水量。结果：脑缺血后脑含水量增加，再灌流后加重脑水肿；线粒体呼吸Ⅲ态及ＲＣＲ于脑缺血时均降低，再灌流早期代偿性升高，再灌流６ｈ后呼吸Ⅳ态明显升高，而呼吸Ⅲ态未恢复，导致ＲＣＲ进一步下降。结论：脑缺血及再灌流均造成脑水肿，线粒体呼吸功能于脑缺血时受抑制，再灌流使线粒体功能进一步受损，无效耗氧增加，提示线粒体功能的改变是再灌流损伤的病理基础之一。
Objective: To explore the relationship between mitochondrial respiratory function and cerebral edema after cerebral ischemia and reperfusion. Methods: Clark oxygen electrode method was used to determine the mitochondrial respiratory state Ⅲ and Ⅳ and respiratory rate (RCR) after cerebral ischemia and reperfusion. Brain water content was calculated according to Elis formula by drying method. Results: After cerebral ischemia, brain water content increased, and reperfusion increased brain edema. Mitochondrial respiratory state III and RCR decreased in cerebral ischemia, compensatory increase in early reperfusion, and respiration Ⅳ state after reperfusion increased significantly , While the state of breathing Ⅲ did not recover, leading to further decline in RCR. CONCLUSION: Cerebral edema is induced by both cerebral ischemia and reperfusion. Mitochondrial respiratory function is inhibited during cerebral ischemia. Reperfusion can further impair mitochondrial function and increase oxygen inefficiency. It suggests that the alteration of mitochondrial function is the pathological basis of reperfusion injury one.