| Objective: Hypoxic ischemic brain damage is the most serious complication after neonatal asphyxia .The state of the illness is heavy, the case fatality rate is high. It can lead to permanent neurological disabilities among survivors such as hypophre ,epilepsy and spasm et al. This test is to recognize and confirm the therapeutic action and citicoline by determining superoxide dismutase and malondialdehyde in the cerebrohomogenate and neonatal venous blood so that to instruct how to treat hypoxic ischemic encephalopathy in clinic.Method: 80 SD young mice, 7 days old, weight from 12 to 20g, divided randomly into control, HIBD model, CTL, RSMi, RSM2, RSM'1 RSM' 2 groups. The HIBD model and the treatment groups all were ligated the left carotid artery and then put in the 37C pot with N292%, O28% gas for 2 hours. CTL group were treated with CTL on dose of 5mg/10g by abdominal administration. RSM1 and RSM'1i groups were administrated 150mg/10g by abdominal cavity. RSM2 and RSM' 2 groups were treated on the dose of 15mg/10g by abdominal administration. All were treated once a day, lasted for 3 days. At the 4th day the rats were killed to be observed the changes of their brain pathology and examined SOD and MDA; Neonates with weight from 2000 to 4400g, gestational ages from 34w to 41 w and days in hospital from 7 to 14 days were divided randomly into normal, nontreatment and treatment groups. The treatment group was administrated 4 to 6ml RSM in 5% or 10% glucose 30ml on the base of routine treatment, once a day, lasted for 7 to 14 days.The nontreatment group was only given routine treatment. Following SOD and MDA in femoral venous blood were examined before and after the treatment. Normal group were punctured in femoral vein in 1 hour afterbirth and before being discharged from hospital.Results: 1.changes of brain pathology The cerebrostructure and cells of rats in control group are normal. In model group the nervous cells are acidophily, parts of cells karyopaknosis, cytoplasm hyperchromic , structure is not clear, and have lymphocyte out of blood vessel and the hyperplasal blood vessel. The cerebrostructure and cells in RSMi is clear, the edema of cell is relieved and the lymphocyte is less than model. The cerebrostructure and cells in RSM2 is not very clear, still have lymphocyte out of blood vessel and the hyperplasal blood vessel. RSM' 1 compare to RSMi, the structure in the former is not clear and the lymphocyte is more. And RSM' 2 compare to RSM2, the structure is not clear and the lymphocyte is more ,still have hyperplasic blood vessel. 2.MDA (1)7 days old young rats MDA in model group is significantly higher than control group (P<0.05), in the treatment groups including CTL ,RSM1, RSM' 1, RSM2 and RSM 2 groups MDA is significantly lower than model group(P<0.05), in the treatment groups excluding RSM' 1 MDA is not significantly different compare to the control group, MDA in CTL is significantly higher than RSM1 group (P<0.05). (2) clinical test MDA in nontreatment group is significantly higher than normal group (P<0.05), there is not significant difference between treatment different between the two group before treating but significantly different between the two group after treating. 3.SOD (1) 7 days old young rats SOD of model group is significantly lower than control group (P<0.05), and there is not significant difference between model and the treatment groups excluding CTL and RSMi groups(PX).05). In CTL and RSMi groups SOD is significantly higher than model group (P<0.05), but still lower than control group(P<0.05). And SOD in CTL group is not significantly different compare to RSM1 group(P>0.05). (2) clinical test SOD in nontreatment group is significantly different compare to normal group. There is not significant difference between treatment group and nontreatment group before treating but significantly different between the two groups after treating.Conclusions: 1. SOD of the HIBD model rats is significantly low, and MDA is very high. In pathology the nervous cells are acidophily, parts of cel...
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