| Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress. | |
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MedLine Citation:
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PMID: 16990481 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Chin Leong Lim; Gary Wilson; Lindsay Brown; Jeff S Coombes; Laurel T Mackinnon |
Publication Detail:
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Type: Journal Article Date: 2006-09-21 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 292 ISSN: 0363-6119 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2007 Jan |
Date Detail:
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Created Date: 2007-01-01 Completed Date: 2007-02-08 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R186-94 Citation Subset: IM |
Affiliation:
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School of Human Movement Studies, University of Queensland, Brisbane, Queensland, Australia. limcl@dso.org.sg |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Alanine Transaminase
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blood Animals Anti-Inflammatory Agents / pharmacology Aspartate Aminotransferases / blood Cytokines / metabolism Dexamethasone / pharmacology Endotoxemia / physiopathology* Heat Stress Disorders / physiopathology* Hot Temperature / adverse effects* Inflammation / chemically induced, physiopathology* Injections, Intramuscular Interleukin-1beta / blood Interleukin-6 / metabolism Irritants Lipopolysaccharides / blood, toxicity Male Rats Rats, Wistar Survival Analysis Tumor Necrosis Factor-alpha / metabolism Turpentine |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents; 0/Cytokines; 0/Interleukin-1beta; 0/Interleukin-6; 0/Irritants; 0/Lipopolysaccharides; 0/Tumor Necrosis Factor-alpha; 50-02-2/Dexamethasone; 8006-64-2/Turpentine; EC 2.6.1.1/Aspartate Aminotransferases; EC 2.6.1.2/Alanine Transaminase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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