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 degrees C rise in T(b); no hypothermia occurred when IPH ceased. Long IPH caused vasodilation and hyperthermia of a comparable magnitude (1.4 degrees C) that were followed by a T(b) fall to 1.9 degrees C below the preheating value. In experiment 2, the Tb-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)degrees C and 39.2 (SEM 0.2)degrees 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)degrees 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.