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The laboratory rat has been used as an animal model to investigate the effects of cocaine on body temperature and to determine if abuse of the drug is a risk factor in the pathogenesis of exercise-induced heat stroke. Animals were trained to run on a treadmill which was enclosed so that the ambient temperature could be regulated. Exercise at ambient temperatures of 20 and 30 degrees C led to a similar rise in core temperature of approximately 1 degrees C, although the starting core temperature was higher in the rats at 30 degrees C (38.5 +/- 0.10 degrees C compared to 37.9 +/- 0.06 degrees C). Cocaine (20 mg/kg) led to a transient fall in core temperature in the 20 degrees C group; the temperature then rapidly recovered, so that after 60 min exercise there was no significant difference between these and the control animals. At the higher ambient temperature cocaine augmented the rise in core temperature during running, although the animals had regained thermal balance by 30 min and core temperature was maintained at 40.2 +/- 0.13 degrees C until the end of the exercise period. The dopamine D1 receptor antagonist SCH 23390 (0.1, 0.3 or 1.0 mg/kg) led to suppression of spontaneous motor activity so that the rats could be persuaded to exercise for only 30-45 min after treatment. Pretreatment with the antagonist did not affect the rise in core temperature induced by cocaine at 30 degrees C which again stabilized by 30 min at 40.0 +/- 0.12 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Ethanol (0.5-3.2g x kg-1 i.p.) caused a dose-dependent fall in body temperature in rats. A dose of 1.5g x kg-1 i.p. led to a fall of 1.6 +/- 0.20 degrees C over 60 min at an environmental temperature of 18 +/- 1 degrees C. There was no evidence of acute tolerance when the hypothermic response was elicited by the same dose of ethanol (0.7--20.0g x kg-1 i.p.) 24 h later; indeed the second response was consistently, although not significantly, greater than the first. Behavioral thermoregulatory studies indicated that the fall in temperature after ethanol is due, at least in part, to a downward setting in the thermoregulatory set point. These results suggest that the rat may be a suitable animal model for a study of accidental hypothermia following ethanol ingestion and exposure to low environmental temperatures.