HYPERTHERMIA DELAYED BY 24 HOURS AGGRAVATES NEURONAL DAMAGE IN RAT HIPPOCAMPUS FOLLOWING GLOBAL-ISCHEMIA

We investigated whether moderate, transient whole-body hyperthermia (c ongruent to 39.6 degrees C), if imposed 1 day following a brief episod e of forebrain ischemia, would affect the neuropathologic outcome. For ty-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 o f one subgroup were placed into a hyperthermic chamber containing high -intensity lamps designed to elevate rectal temperature to 39 to 40 de grees C for 3 hours. Normothermic subgroups received the same procedur es, but the heating lamps were turned off. Eight days after brain isch emia or the sham procedure, brains were perfusion-fixed, and numbers o f ischemic-appearing CA1 pyramidal neurons were counted. In rats with 7-minute forebrain ischemia, delayed hyperthermia increased mean numbe rs of ischemic neurons by 2.6- to 2.7-fold in all subsectors of area C A1 (p < 0.05, ANOVA). Delayed hyperthermia in 5-minute ischemic rats a lso tended to increase mean numbers of ischemic neurons (by Ii-fold in lateral, B-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-m inute global ischemic insult, exacerbates the extent of ischemic neuro nal injury.