Summary:We have tested whether small intraischemic variations in brain temperature influence the outcome of transient ischemia. To measure brain temperature, a ther mocouple probe was placed stereotaxically into the left dorsolateral striatum of rats prior to 20 min of four-vessel occlusion. Rectal temperature was maintained at 36-37°C by a heating lamp, and striatal temperature prior to ischemia was 36°C in all animals. Six animal subgroups were investigated, including rats whose intraischemic striatal brain temperature was not regulated, or was maintained at 33, 34, 36, or 39°C. Postischemic brain tem perature was regulated at 36°C, except for one group in which brain temperature was lowered from 36°C to 33°C during the first hour of recirculation. Energy metabolites were measured at the end of the ischemic insult, and his topathological evaluation was carried out at 3 days after ischemia. Intraischemic variations in brain temperature had no significant influence on energy metabolite levels measured at the conclusion of ischemia: Severe depletion of brain ATP, phosphocreatine, glucose, and glycogen and elevation of lactate were observed to a similar degree in all experimental groups. The histopathological conse quences of ischemia, however, were markedly influenced by variations in intraischemic brain temperature. In the Despite the utility of small animal models of global ischemia, several groups have noted vari ability of outcome from animal to animal (Payan et aI., 1965;Furlow, 1982; Blomqvist et aI., 1984; Harrison et aI., 1985; Vibulsresth et aI., 1987). Al though these variations, in part, may be the conse quence of differences in the severity of ischemia it-
729hippocampus, CA I neurons were consistently damaged at 36°C, but not at 34°C. Within the dorsolateral striatum, ischemic cell change was present in 100% of the hemi spheres at 36°C, but in only 50% at 34°C. Ischemic neu rons within the central zone of striatum were not ob served in any rats at 34°C, but in all rats at 36°C. In rats whose striatal temperature was not controlled, brain tem perature fell from 36 to 30-31°C during the ischemic in sult. In this group, no ischemic cell change was seen within striatal areas and was only inconsistently docu mented within the CAl hippocampal region. These re sults demonstrate that (a) rectal temperature unreliably reflects brain temperature during ischemia; (b) despite severe depletion of brain energy metabolites during isch emia at all temperatures, small increments of intra ischemic brain temperature markedly accentuate histo pathological changes following 3-day survival; and (c) brain temperature must be controlled above 33°C in order to ensure a consistent histopathological outcome. Low ering of the brain temperature by only a few degrees during ischemia confers a marked protective effect. Key Words: Ischemia-Brain temperature-Rats-Hypo thermia.self, other factors not directly related to the pri mary insult may also play an important role in determining the ultimate histopathological out come.Recen...