• R C Baena, R Busto, W D Dietrich, M Y Globus, and M D Ginsberg.
• Department of Neurology, University of Miami School of Medicine, FL 33101, USA.
• Neurology. 1997 Mar 1;48(3):768-73.

AbstractWe investigated whether moderate, transient whole-body hyperthermia (approximately 39.6 degrees C), if imposed 1 day following a brief episode of forebrain ischemia, would affect the neuropathologic outcome. Forty-two Wistar rats were subjected to either a 5- or 7-minute period of bilateral common carotid artery occlusion plus hypotension (50 mm Hg), or to the equivalent sham procedure. Twenty-four hours later, rats of one subgroup were placed into a hyperthermic chamber containing high-intensity lamps designed to elevate rectal temperature to 39 to 40 degrees C for 3 hours. Normothermic subgroups received the same procedures, but the heating lamps were turned off. Eight days after brain ischemia or the sham procedure, brains were perfusion-fixed, and numbers of ischemic-appearing CA1 pyramidal neurons were counted. In rats with 7-minute forebrain ischemia, delayed hyperthermia increased mean numbers of ischemic neurons by 2.6- to 2.7-fold in all subsectors of area CA1 (p < 0.05, ANOVA). Delayed hyperthermia in 5-minute ischemic rats also tended to increase mean numbers of ischemic neurons (by 11-fold in lateral, 6-fold in middle, and 5-fold in medial CA1 subsectors), but these differences were not statistically significant. We conclude that moderate, transient hyperthermia, even if occurring 1 day after a 7-minute global ischemic insult, exacerbates the extent of ischemic neuronal injury.

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