Abstract： Objective To observe the effects of hyperbaric oxygen(HBO)on peroxidative damage and apoptosis induced by focal cerebral ischemia and reperfusion(CI/R)in rats,and to further investigate the effects of HBO on CI/R-induced damage and the mechanism involved.Methods Eighty SD rats were randomly divided into 4 groups:the sham control group(n=8),the cerebral ischemia/reperfusion group(or the CI/R group,n=24),and the cerebral ischemia/reperfusion plus normal oxygen breathing group(or the CI/R+N group,n=24),the cerebral ischemia/reperfusion plus HBO group(or the CI/R+HBO group,n=24).The focal cerebral ischemia and reperfusion rat model was developed by using the middle cerebral artery occlusion method(MCAO).The animals in the control and the CI/R groups were left there without any treatment after surgery.The animals in the CI/R+N group breathed oxygen under normal pressure,30 min after surgery,while the animals in the CI/R+HBO group received routine HBO treatment 30 min after surgery,with 60 min a session for a duration of 12 h.Eight animals of each group were killed at hour 12,24 and 48,following surgery,for collection of CI/R-damaged focal cerebral tissue.Colorimetric method was used to monitor the activity of mitochondrial superoxide dismutase(SOD)in the brain tissue and the content of malondialdehyde(MDA),and cell flowmetry was applied to detect apoptosis of brain cells.Results The activity of SOD in the CI/R group decreased continuously at hour 12,24 and 48,and was significantly lower than that of the control group(P＜0.01).The activity of SOD in the CI/R+N group at hour 12,24 and 48 was obviously higher than that of the CI/R group(P＜0.05),and the activity of SOD in the CI/R+HBO group at hour 12,24 and 48 was significantly higher than those of the CI/R group and the CI/R+N group(P＜0.05),indicating that HBO could most effectively protect the activity of SOD in mitochondria,following cerebral ischemia induced by reperfusion.After surgery,the content of MDA for the CI/R group increased continuously at hour 12,24 and 48,and was significantly higher than that of the control group(P＜0.01).The contents of MDA for the CI/R+N group at hour 12,24 and 48 were lower than those of the CI/R group,but without statistical significance(P＜0.05).The contents of MDA for the CI/R+HBO group at hour 12,24 and 48 were all significantly lower than those of the CL/R group(P＜0.01),indicating that HBO could effectively inhibit the production of MDA.After surgery,apoptosis of brain cells at hour 12,24 and 48 for the CI/R group increased continuously,and was significantly higher than that of the control group(P＜0.01).Apoptosis of brain cells at hour 12,24 and 48 for the CI/R+N group was lower than that of the CI/R group(P＞0.05),but without statistical significance(P＜0.05).Apoptosis of brain cells at hour 24 and 48 for the CI/R+HBO group was significantly lower than that of the CI/R group and the CI/R+N group at hour 48(P＜0.05),indicating that HBO could effectively alleviate apoptosis of brain cells following cerebral ischemia induced by reperfusion.Conclusions HBO could obviously increase the stability of mitochondria,effectively protect the activity of SOD of mitochondria in the brain tissue following cerebral ischemia induced by reperfusion,alleviate peroxidative mitochondrial damage induced by ischemia reperfusion.All this indicated that HBO was obviously more effective than normal oxygen breathing in the protection of the injured brain.