Stroke, Vol 21, 1318-1325, Copyright © 1990 by American Heart Association
WD Dietrich, R Busto, I Valdes and Y Loor
We compared the neuropathological consequences of global forebrain ischemia
under normothermia versus mild hyperthermia. Twenty-one rats underwent 20
minutes of four-vessel occlusion during which brain temperature was
maintained at either 37 degrees C (normothermia, n = 9) or 39 degrees C
(hyperthermia, n = 12). Quantitative neuropathological assessment was
conducted 1 or 3 days later. At 1 day following the ischemic insult,
normothermic rats demonstrated neuronal injury mainly confined to the most
dorsolateral striatum. By 3 days, ischemic cells were present throughout
the striatum and CA1 hippocampus in normothermic animals. Compared with
normothermic rats, intraischemic hyperthermia significantly increased the
extent and severity of brain damage at 1 day after the ischemic insult.
Areas of severe neuronal necrosis and frank infarction included the
cerebral cortex, CA1 hippocampus, striatum, and thalamus. Morphologic
damage was also detected in the cerebellum and pars reticulata of the
substantia nigra. An overall mortality rate of 83% was demonstrated at 3
days in the hyperthermic ischemic group. We conclude that intraischemic
hyperthermia 1) markedly augments ischemic brain damage and mortality
compared with normothermia, 2) transforms ischemic cell injury into frank
infarction, and 3) accelerates the morphological appearance of ischemic
brain injury in regions usually demonstrating delayed neuronal necrosis.
These observations on mild hyperthermia may have important implications for
patients undergoing cardiac or cerebrovascular surgery as well as patients
following cardiac arrest or those with stroke-in- evolution.
ARTICLES
Effects of normothermic versus mild hyperthermic forebrain ischemia in rats
Department of Neurology, University of Miami School of Medicine, Fla. 33101.
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