Stroke, Vol 18, 464-471, Copyright © 1987 by American Heart Association
DS Warner, ML Smith and BK Siesjo
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.
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Ischemia in normo- and hyperglycemic rats: effects on brain water and electrolytes
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