Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress
Article
Article Title | Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress |
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ERA Journal ID | 3151 |
Article Category | Article |
Authors | Lim, Chin Leong (Author), Wilson, Gary (Author), Brown, Lindsay (Author), Coombes, Jeff S. (Author) and Mackinnon, Laurel T. (Author) |
Journal Title | American Journal of Physiology: Regulatory, Integrative and Comparative Physiology |
Journal Citation | 292 (1), pp. R186-R194 |
Number of Pages | 9 |
Year | 2007 |
Place of Publication | Bethesda, MD. United States |
ISSN | 0363-6119 |
1522-1490 | |
Digital Object Identifier (DOI) | https://doi.org/10.1152/ajpregu.00921.2005 |
Web Address (URL) | http://ajpregu.physiology.org/content/292/1/R186.full.pdf+html |
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 2h after receiving the respective treatments, followed by heat exposure until the core temperature (Tc) was 42°C for 15min; 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 Tc 40°C (T40), and 15 min after achieving Tc 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. |
Keywords | dexamethasone; inflammation; turpentine |
ANZSRC Field of Research 2020 | 320801. Cell physiology |
320102. Haematology | |
320699. Medical biotechnology not elsewhere classified | |
Public Notes | First published 21 Sep 2006 |
Byline Affiliations | University of Queensland |
Institution of Origin | University of Southern Queensland |
https://research.usq.edu.au/item/q0w44/pre-existing-inflammatory-state-compromises-heat-tolerance-in-rats-exposed-to-heat-stress
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