Heat defense control in an experimental heat disorder

Both whole-body heat exposure and intraperitoneal heating (IPH) result in a body temperature (T-b) fall that occurs once heating is abated ("hyperther mia-induced hypothermia"). This phenomenon involves a decrease in the thres hold T-b (Tb-thresh) for activation of metabolic heat production (cold defe nse). Whether the T-b-thresh for ear skin vasodilation (heat defense) also changes during hyperthermia-induced hypothermia remains unknown. In experim ent 1, we applied IPH to guinea pigs by perfusing water through a preimplan ted intraperitoneal thermode and delivered the total heat load of either ap proximately 1.5 kJ ("short" IPH, perfusion duration: 14 min) or approximate ly 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 tw ice: at the beginning of long IPH and at the nadir of the post-IPH hypother mia. The two Tb-thresh values were 39.0 (SEM 0.1)degrees C and 39.2 (SEM 0. 2)degrees C respectively. In the controls, the Tb-thresh was measured at th e beginning and after short IPH, both control values were 39.0 (SEM 0.2)deg rees C. We conclude that the hyperthermia-induced hypothermia. although pre viously shown to be coupled with a decrease in the Tb-thresh for cold defen se, occurs without any substantial change in the Tb-thresh for heat defense . We speculate that postheating thermoregulatory disorders are associated w ith threshold dissociation, thus representing the poikilothermic (wide dead -band) type of T-b control.