Glucocorticoids and hypothermic induction and survival in the rat

Glucocorticoids (GC) are important for thermoregulatory responses to low environmental temperatures. Pretreatment of hamsters, which are capable of natural hibernation, with cortisone acetate has been demonstrated to improve carbohydrate homeostasis during hypothermia. The objectives of the current studies were to evaluate the effects of GC pretreatment of a nonhibernator, the rat, on (i) cooling time, (ii) carbohydrate homeostasis (in terms of liver and cardiac glycogen concentrations and plasma glucose concentration), and (iii) duration of survival in hypothermia. In addition, the effects of liver glycogen depletion on cooling times and survival were examined. Hypothermia was induced in rats by exposure to a helium:oxygen (80:20, Helox) atmosphere at 0 degree C. Pretreatment of rats with triamcinolone acetonide (1.5 mg/kg/day, sc, 48, 24, and 1 hr prior to induction) significantly (P less than 0.05) lengthened induction time, while fasting was associated with a significant decrement (25%). While liver and cardiac glycogen levels in control and GC-treated rats fell approximately 45% during cooling, this reduction occurred over a significantly greater period of time in treated rats and suggests a sparing of glycogen or increased capacity for its production in response to GC. Glycogen utilization was accompanied by a hyperglycemia in control, GC-treated, and fasted groups. Survival in hypothermia at a rectal temperature of 14-15 degrees C in GC-treated (9.5 +/- 1.2 hr) and fasted (10.9 +/- 0.9 hr) rats was not significantly different from control (10.5 +/- 1.1 hr) values. These findings suggest that treatment with GC can increase the thermogenic capacity of the rat (as evidenced by an increased induction time) and promote carbohydrate homeostasis, but does not contribute to an enhancement of survival in the hypothermic nonhibernator.