Heat defense control in an experimental heat disorder

Abstract 

Both whole-body heat exposure and intraperitoneal heating (IPH) result in a body temperature (T _b) fall that occurs once heating is abated (”hyperthermia- induced hypothermia”). This phenomenon involves a decrease in the threshold T _b (T _b-thresh) for activation of metabolic heat production (cold defense). Whether the T _b-thresh for ear skin vasodilation (heat defense) also changes during hyperthermia-induced hypothermia remains unknown. In experiment 1, we applied IPH to guinea pigs by perfusing water through a preimplanted intraperitoneal thermode and delivered the total heat load of either approximately 1.5 kJ (”short” IPH; perfusion duration: 14 min) or approximately 3.0 kJ (”long” IPH; 40 min). Short IPH caused skin vasodilation and a 1.1°C rise in T _b; no hypothermia occurred when IPH ceased. Long IPH caused vasodilation and hyperthermia of a comparable magnitude (1.4°C) that were followed by a T _b fall to 1.9°C below the preheating value. In experiment 2, the T _b-thresh for skin vasodilation was measured twice: at the beginning of long IPH and at the nadir of the post-IPH hypothermia. The two T _b-thresh values were 39.0 (SEM 0.1)°C and 39.2 (SEM 0.2)°C respectively. In the controls, the T _b-thresh was measured at the beginning and after short IPH; both control values were 39.0 (SEM 0.2)°C. We conclude that the hyperthermia- induced hypothermia, although previously shown to be coupled with a decrease in the T _b-thresh for cold defense, occurs without any substantial change in the T _b-thresh for heat defense. We speculate that postheating thermoregulatory disorders are associated with threshold dissociation, thus representing the poikilothermic (wide dead-band) type of T _b control.