Abstract

In the rat heat stroke model, established by heating to a climatic chamber temperature of 42 degrees C, the brain temperature was found to be consistently lower than the rectal temperature, suggesting efficient brain cooling mechanisms in the rat. In response to heating, with increasing brain temperature, the latencies of the somatosensory evoked potentials (SEPs) showed an initial decrease followed by an increase (inflection point). Studies were done on rats heated up to, before, or after the inflection point and then cooled. Reversibility with cooling of functional and structural changes induced by heat was evaluated by analysis of SEPs, survival time, brain blood perfusion and histopathology. The evidence from these studies demonstrated that the brain temperature at which the inflection in wave P2 latency occurred was critical, beyond which hyperthermia produced irreversible changes in the SEP, shorter survival time, relative reduction in brain blood perfusion and evidence of brain histopathological damage. The suggestion that endorphins may mediate brain dysfunction in hyperthermia was investigated. In rats heated and then cooled after wave P2 latency inflection naloxone, the endorphin antagonist, was injected (10 mg/kg, intravenously) just prior to the inflection. It produced reversibility of SEP changes as well as longer survival time (P less than 0.001) compared to saline-treated rats.