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 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.
Lim
Chin Leong
CL
School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia. limcl@dso.org.sg
Wilson
Gary
G
Brown
Lindsay
L
Coombes
Jeff S
JS
Mackinnon
Laurel T
LT
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
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