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Previous investigations have shown that preischemic hyperglycemia worsens cerebral outcome. This study sought to delineate the temporal relations between postischemic brain edema and the development of spontaneous epileptic activity. Fasted rats were subjected to 10 minutes of forebrain ischemia. One-half of the animals were made hyperglycemic by glucose infusion prior to ischemia. At serial recirculation intervals regional specific gravity and cortical electrolytes were measured. Normoglycemic animals showed a biphasic increase in brain water content that was fully resolved by 96 hours and had no convulsive activities. Hyperglycemic brains, although displaying a slower resolution from an initial transient decrease in specific gravity, also developed an interval with normal water content that persisted at 18 hours postischemia. At 24 hours, an increase in water content recurred and was soon followed by the onset of seizure activity. Cortical electrolyte changes were unremarkable until seizures occurred. Significant increases in total Na+, Cl-, and Ca2+ and a decrease in K+ were then seen. We conclude that while the normoglycemic brain is capable of resolving postischemic edema in this model, the hyperglycemic brain develops a delayed secondary increase in water content followed by the onset of seizure activity accompanied by a deterioration of ionic homeostasis.

Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes.