| Background and objectives: Intracerebral hemorrhage (ICH) is one of the frequently-occurring disease of the nervous system. Brain edema is one of the important reasons of its high mortality. The oxcidative stress and the overflow of ca2+ in nervous cells are the biochemical foundation of brain edema. N-Methyl-D-Aspartate(NMDA) ,a special nervous mediator, is reported to have close relationship with overflow of ca2+ , which in turn increase the production of free radicals, worsen brain edema,eventurally cause the death of neurons. However, whether the inhibitor of NMD A (ketamine) can reduce the volume of brain edema and decrease the formation of free radicals throught inhibiting NMDA receptor is still under further research.We investigate the change in free radicals, SOD ,the volume of brain edema after ICH hi different time span. The role of the inhibitor of NMDA receptor is also examined in our study. The vitality of SOD can reflex the ability of self-body , the level of MDA can reflex the extent to which free radicals attack nervous cells. These help to illustrate the mechanism of brain edema after ICH, provide theoretical basis for brain edema.Materiab and methods: (1) 60 healthy SD rats were distributed into two part. Part 1: 30 healthy SD rats were distributed into 5 groups, (the divide of groups is based on the different time of ICH, 8h-120h, respectively) The rats were infused self body blood, followed injecting normal saline(180mg/kg) into abdomen of rats after one hour. Part 2: 30 healthy SD rats were also distributed into 5 groups. The rats were infused self body blood, followed injecting ketamine(180mg/kg) into abdomen of rats after one hour. Needles were inserted into the right caudate nuclears using stereo tactic guidance. Each groups were infused in 10-15 minutes and detained for 20minutes until needle was removed.(2) The rats were sacrificed by decapitation at 8h,24h,48h,72h,120h respectively after the operation. Removed the operation side cerebral hemisphere, cut two coronal slices of brain tissue centered with the needle passage, each slice approximately 1.5mm thick, The slice hi front of the needle passage was sacrificed to investigate the content of brain water; The other slice was sacrificed to determine the volume of SOD, MDA through violet spectra-meter. The data were handled with spss 10.0 statistic sofhnare. The difference of two groups was compared with one-way analysis of variance and LSD. significant level is a =0.05. Result: 1. After the operation, all the animals behaved low spirit ,low ability of self-clearance and equilibration, eat little, the myodynamia of left extremities decrease and occured spin, etc. some of them sezusing.2. The results of brain water content: The differences between rats in these two parts in comparative time are significant(P<0.05), demonstrating ketamine can reduce the volume of brain edema in different time span.3. The contents of SOD and MDA: SOD: group A: 328.5 8.83, B: 315.5 15.9, C: 297.2 23.9, D: 244.9 28.1, E: 253.1 27.7, F: 363.8 11.6, G: 353.8 12.7, H: 322.1 10.6,1: 279.9 12.6, J: 313.2 32.3. MDA: group A:2.73 0.22, B: 3.00 0.18, C: 3.12 0.07, D: 3.58 0.16, E: 3.08 0.92,F: 2.53 0.20 G: 2.64 0.11, H: 2.79 0.17, I: 2.94 0.13, J: 2.80 0.24. the volume of SOD decreased after ICH whereas the volume of MDA rised. The differences between A and F; B and G; C and H; D and I; E and J are significant(P<0.05), demonstrating ketamine can reduce the volume of MDA and increase SOD in different time span.Conclusions:1. stereo orientation injection method was adopted to malie intracerebral hemorrhage model in this research. This method had the accurate localization, the high rate of success and standardization.2. Free radicals can cause severe brain edema. The vitality of SOD decreased after the edema and the bottom is 72h. the change of MDA is different from that of SOD.3. The inhibitor of NMDA receptor, ketamine, can effectively reduce the formation of free radicals and brain edema.
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