Stroke, Vol 24, 111-116, Copyright © 1993 by American Heart Association
WD Dietrich, O Alonso and R Busto
BACKGROUND AND PURPOSE: Clinical and experimental data indicate that
hyperglycemia can aggravate the consequences of stroke and cerebral
ischemia. The purpose of this study was to examine the effects of moderate
hyperglycemia on the response of the blood-brain barrier to normothermic
(37 degrees C) and hypothermic (30 degrees C) global forebrain ischemia.
METHODS: Sixteen rats underwent 20 minutes of four- vessel occlusion
followed by 30 minutes of postischemic recirculation. We used the protein
tracer horseradish peroxidase as an indicator of increased vascular
permeability, and rats were perfusion-fixed for microscopic analysis. To
produce moderate hyperglycemia, we gave an intraperitoneal injection of 50%
dextrose 15 minutes before the ischemic insult. RESULTS: After normothermic
brain ischemia, normoglycemic rats (plasma glucose level, 115 +/- 3 mg/dl)
demonstrated extravasated horseradish peroxidase mainly restricted to the
cerebral cortex. In contrast, more severe and widespread protein
extravasation was documented throughout the neuraxis of hyperglycemic
(plasma glucose level, 342 +/- 27) rats. Sites of protein leakage included
the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum. Foci
of protein extravasation were associated with pial and large penetrating
vessels. Intraischemic hypothermia significantly attenuated the blood-
brain barrier consequences of hyperglycemic brain ischemia. CONCLUSIONS:
Under normothermic ischemic conditions, hyperglycemia significantly worsens
the degree of acute blood-brain barrier breakdown compared with
normoglycemia. Postischemic blood-brain barrier disruption may play an
important role in the pathogenesis of increased brain damage associated
with systemic hyperglycemia.
ARTICLES
Moderate hyperglycemia worsens acute blood-brain barrier injury after forebrain ischemia in rats
Department of Neurology, University of Miami School of Medicine, FL 33101.
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