ABSTRACT
Objective The hypoxic-ischemic(HI) cardio-cerebral damage caused by cardiac arrest in perioperative period is the main cause of acute and chronic disability in children patients.To investigate role of mitochondrial dysfunction in hypoxic-ischemic brain damage of mice.Methods The hypoxic-ischemic mice model was established by the bilateral carotid artery occlusion and hypoxia treatment.The neurobehavior of mice in HI model group,sham-operated group,and comparative group were evaluated within 48 hours after operation.After 48 hours,the mice were killed to evaluate the brain water content,mitochondria content,swelling,antioxidant capacity,and respiratory function.Results Within 0,24 hours after operation,the abnormal rate of the neurobehavior of HI model mice was 83.33％,which was significantly higher than comparative and sham-operated groups.The water content of right brain was significantly increased evidently compared to the other two groups (P ＜ 0.05).The content and swelling of mitochondria in brain were increased.The activity of superoxide dismutase (SOD),the glutathione (GSH) content,respiratory state 3 (ST3),and respiration control of rate (RCR) were significantly decreased; while the content of malondialdehyde (MDA) and ST4 were significantly increased (P ＜ 0.05).Conclusions The brain tissue showed different swelling,the mitochondrial function occurred disorder,which might play an important role in hypoxic-ischemic brain damage of mice.