Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T + HE), dexamethasone (D + HE), and turpentine and dexamethasone combined (TD + HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (T-c) was 42 C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment (baseline I), after 2 h of passive rest (baseline II), at T-c 40 degrees C (T40), and 15 min after achieving T-c 42 degrees C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD + HE rats (37.5%), followed by the HE (62.5%), T + HE (75%), and D + HE (100%) rats (P < 0.05). The duration of survival at T42 C was shortest in the TD + HE rats (9.9 +/- 6.2 min) (P < 0.01), followed by the T + HE (11.3 +/- 6.1 min) and the HE (12.2 +/- 4 min) (P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T + HE (352%) and HE (178%) rats (P < 0.05). D + HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.