effects of a free radical scavenger on spinal cord injury after transient ischemia in rabbits *
Oxygen- free radical species play detrimental roles in ischemia and postreperfusion injuries. In this study, the author examined the effect edaravone（3-methyl-1-phenyl- 2-pyrazolin-5-one），a free radical scavenger, on hindlimb motor function and histopathology after a transient episode of spinal cord ischemia in an animal model. Twenty-two Japanese white rabbits underwent spinal coed ischemia by occlusion of the aorta distal to the origin of the left renal artery for 20 min using a balloon inflation technique. The animals were assigned to four groups: a sham group（catheter placement without balloon inflation; n= 4），a control group（ischemia followed by 3ml saline i. v. injection 30 min after reperfusion with a 48 hr recovery period; n= 6），and E48H and E7D group（ischemia followed by 3 mg/kg edaravone injection 30 min after reperfusion, with 48 hr and 7 day recovery periods, respectively; n= 6 in each group）．Hindlimb motor function was assessed during the recovery periods. The histopatology of the lumbar spinal cord was also examined. All animals in the control group became paraplegic with marked histopathologic changes such as significant motor neuron cell loss, nuclear membrane fragmentation and vacuoles in the lumbar spinal cord. In both edaravone-treated groups, hindlimb motor function was better preserved for 48 hr and 7 days than in the control group. When compared with the control group, the edaravone-treated groups had significantly greater numbers of normal neurons in the anterior spinal cord（6±12, 38.2±40 and 24±19, control group, H48H group and E7D group, respectively）．While the mean motor neuron area in the animals of the E48H group was greater than that of those in the sham group, it became smaller in the animal of the E7D group（113 ±117, 408±298, 267±159 and 377±23, control group, H48H group, E7D group and sham group, respectively）．In addition, ischemic neuron along with normal neurons were observed in the animals of the E7D group. These histopathologic findings of edaravone-treated groups are compatible with neuronal cellular edema at 48 hrs and a partial neuronal death at 7 days postischemia. The results of this study suggest that edaravone provides a partial protection against 20 min ischemic spinal cord injury in rabbits, but that delayed neuronal death cannot be completely prevented. (Accepted on October 30, 2008)
