The Effect Of Neuroprotective Drugs On Nitro Oxide After Cerebral Ischemia

Part 1:Establishment and improvement of the middle cerebral artery(MCA)occlusion modelTo establish the MCA occlusion model and upgrade its operation and evaluation.We choked the MCA of rat by a suitable strand to cause infarct in corresponding encephalic regions,and then removed brain and sliced at 24h after ischemia.Brain slices were drained by TTC to judge if the models were successful.We upgraded operation and the strand to improve the achievement of model.Objective signs of all rats were recorded to be compared with the results of TTC stained.Injury regions were white and normal regions were ret after TTC stained.The model that had white brain regions was successful. According to the results of TTC strained,the achievement ratio of upgrading group was 71.67%and original group was 52.0%.Evaluating models by objective signs had high sensitivity but low specificity.We has successfully established the MCA occlusion model and improved its achievement ratio by upgrading.Objective signs will cause high false positive,thus we suggest parts of them should be deleted.Part 2:The charge of nitro oxide after cerebral ischemia,and effect of drugs(monosialoganglioside and nimodipine)on itTo observe the charge of neuronal nitro oxide synthase (nNOS),induced nitro oxide synthase(iNOS)and nitro oxide(NO),and study the neuroprotection of monosialoganglioside and nimodipine against them.Using middle cerebral artery occlusion model by thread occlusion method,We observed nNOS activity,iNOS activity and NO content at 30min,2h,6h and 24h after ischemia.Then we study the effect of monosialoganglioside on iNOS and nimodipine on nNOS respectively and their neuroprotection.The nNOS activity increased at 30min and reduced later;The iNOS activity increased at 24h;The NO content increased both at 30min at 24h. Monosialoganglioside inhibited iNOS activity and nimodipine inbibited nNOS activity respectively after ischemia,and they could light ischemic damage.The nNOS and iNOS activity will increase after ischemia and injure nervous tissue by producing multitudinous NO.Inhibition of them can light ischemic damage.