Abstract
Brain edema was produced in 5- and 30-day-old rats by the intrathecal infusion of tracer doses of inulin labeled with carbon 14 dissolved in microliter volumes of artificial cerebrospinal fluid. The older animal showed a sustained elevation of spinal fluid pressure in association with a marked resistance to penetration of labeled inulin into the brain stem and cerebellum. In contrast, continuous penetration of the extracellular marker into the edematous brain of the 5-day-old rat was found. Pretreatment with dexamethasone completely prevented abnormal fluid accumulation. Additionally, the access route of inulin 14 C to the extracellular space was restored in the older animal, while this influx via the intercellular clefts was only minimally enhanced in the younger animal. An important mechanism of action of dexamethasone may be the prevention of swelling in glia and their processes.
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