Objective : The purpose of the present study was to determine the appropriate time of clinical intervention by observing and analyzing the changes in the size of infarct, penumbra and cerebral edema and the extend of neurological deficit due to reperfusion damage according to time in a reversible cerebral ischemic model of reperfusing blood flow after inducing ischemia by maintaining middle cerebral artery occlusion for 2 hours(h) in rats. Methods : The rats were divided according to reperfusion time into control group(0 h reperfusion time) and experimental groups(0.5, 1, 2, 3, 4, 5, 6, 12, and 24 h of reperfusion time). Results : Changes in the size of infarction due to reperfusion damage were 0.93, 1.48 and 1.16% at 0.5, 1 and 2 h after reperfusion, respectively, and although a statistical significance was not present compared to 1.35% of the control group, damages increased drastically up to 6 h(6.64%), and the size increased were 6.65 and 6.78% at 12 and 24 h, respectively. Also there was no significant difference after 6 h up to 24 h in the size of infarction. In the areas where infarction occurred, reperfusion damage increased significantly with time in cortex than in subcortex. Accordingly, the size of penumbra area also showed a statistically significant decrease from 2 h up to 6 h after reperfusion, and 6 h after reperfusion, the area almost disappeared, becoming permanent infarction. Thus, reperfusion damage showed a significant increase from 2 h up to 6 h after reperfusion, and became steady thereafter. As for the mean ratio of the extend of cerebral edema, the control group and reperfusion 0.5 h group were 1.073 and 1.081, respectively ; up to 2 h thereafter, the ratio decreased to 1.01 but increased again with time ; and in reperfusion 12 h and reperfusion 24 h, the ratios were 1.070 and 1.075, respectively, showing similar size with that of control group. As for neurological deficit scores, the score of the control group was 2.67, that of reperfusion 2 h was 2, those of reperfusion 3 h and 6 h groups were 3.2 and 3.8, respectively, and those of reperfusion 12 h and 24 h groups were 4.2 and 4.6, respectively. Thus, as for the test results, the neurological deficit increased with time 2 h after reperfusion, and in reperfusion 12 and 24 h groups, almost all the symptoms appeared. Conclusion : As shown in these results, although the changes in the size of infarction due to reperfusion damage did not increase up to 2 h after reperfusion in the experimental groups compared to the control group, damage increased significantly thereafter up to 6 h, and the size remained about the same from 6 h to 24 h after reperfusion, becoming permanent infarction ; thus, the appropriate time of intervention according to the present study is at least 6 h before after maintaining reperfusion, including the time of cerebral artery occlusion.