It has been reported that a very high body temperature (hyperthermia) is either detrimental or beneficial to animal and human health. The reasons for these opposing effects of hyperthermia are not clear. However, these conflicting results may be attributed to different experimental conditions used in those studies, e.g., intensity of hyperthermia, duration of hyperthermic condition, severity of secondary stimulation etc.

The present experiments are concerned with the detrimental effects of hyperthermia in animal model of heat stroke. The aim of the present experiments was to examine the hypothesis that the enhanced LPS fever in heat stressed (HS) animals was caused by leaked intestinal bacterial endotoxin. Male rabbits were made transiently hyperthermic (a maximum rectal temperature of 43 °C). They were then allowed to recover in a room of 24 + 1 °C. Results: (1) When intravenously administered with LPS (60 ng/kg, Escherichia coli serotype 0111: B4), one day, but not two days and three days, post - HS rabbits exhibited significantly larger fever (by 34.6 %) than the controls. (2) However, when intravenously challenged with human recombinant interleukin-1beta, the 1 - day post - HS rabbits did not show any enhanced fever. (3) Pretreatment of rabbits with antibiotics significantly attenuated the enhanced LPS fever observed in the 1 - day post HS rabbits. (4) Plasma TNFalpha increased during LPS fever similarly in both the control and 1 - day post - HS rabbits. (5) Levels of plasma corticosterone and osmolality in the 1 - day post - HS rabbits, prior to LPS administration, did not differ from those of the control animals. These results suggest that the transiently enhanced LPS fever in the 1 - day post - HS rabbits may be caused by increased leakage of intestinal endotoxin into blood circulation. The present results also implicate that HS animals are more susceptible to infections. In fact, such suggestion has been reported in earlier clinical case reports.