title: Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress.
abstract: 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 degrees 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 degrees 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.
authors.affiliation: School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia. limcl@dso.org.sg
authors.forename: Chin Leong
authors.initials: CL
authors.lastname: Lim
authors.forename: Gary
authors.initials: G
authors.lastname: Wilson
authors.forename: Lindsay
authors.initials: L
authors.lastname: Brown
authors.forename: Jeff S
authors.initials: JS
authors.lastname: Coombes
authors.forename: Laurel T
authors.initials: LT
authors.lastname: Mackinnon
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001219:Aspartate Aminotransferases / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D019446:Endotoxemia / Q000503:physiopathology*; D018882:Heat Stress Disorders / Q000503:physiopathology*; D006358:Hot Temperature / Q000009:adverse effects*; D007249:Inflammation / Q000139:chemically induced / Q000503:physiopathology*; D007273:Injections, Intramuscular; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000378:metabolism; D007509:Irritants; D008070:Lipopolysaccharides / Q000097:blood / Q000633:toxicity; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D016019:Survival Analysis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014425:Turpentine
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D007509:Irritants; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D003907:Dexamethasone; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D014425:Turpentine