We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.
|Original language||English (US)|
|Number of pages||8|
|Journal||Advances in neurology|
|State||Published - 1990|
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