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Am J Physiol Regul Integr Comp Physiol 292: R186-R194, 2007. First published September 21, 2006; doi:10.1152/ajpregu.00921.2005
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Physiology and Pharmacology of Temperature Regulation

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

¹School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia; ²Defence Medical and Environmental Research Institute, Defence Science Organisation National Laboratories, Singapore; ³School of Biomedical Sciences, University of Queensland, Brisbane, Queensland, Australia

Submitted 30 December 2005 ; accepted in final form 8 September 2006

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°C (T40), and 15 min after achieving T_c 42°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.

inflammation; turpentine; dexamethasone

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