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Am J Med Sci. 2009 Apr;337(4):265-70. doi: 10.1097/MAJ.0b013e31818b0fa2.

Pre-existing lipopolysaccharide may increase the risk of heatstroke in rats.

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Department of Nursing, Nanfang Hospital, Southern University, Guangzhou, Guangdong, China.



: We attempted to ascertain whether pre-existing inflammatory state [caused by exogenous administration of lipopolysaccharide (LPS)] exacerbated multiorgan dysfunction in experimental heatstroke.


: Immediately after the start of heat stress (42 degrees C), anesthetized rats were divided into 2 major groups and given 0.9% NaCl solution (10 mL/kg of body weight, intravenously) or LPS (10 mg/kg of body weight, intravenously). On heat exposure, the occurrence of both hyperthermia (>42.0 degrees C) and hypotension (mean arterial pressure <50 mm Hg) was taken as the time point for heatstroke onset.


: The LPS-treated, but not the saline-treated, animals underwent the heat stress for 52 minutes, displayed heatstroke syndromes. As compared with those of the saline controls, the LPS-treated rats had higher extent of activated inflammation (evidenced by increased plasma levels of interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6), hypercoagulable state (evidenced by increased levels of prothrombin time, activated partial thromboplastin time, and D-dimer, but decreased levels of both protein C and platelet counts), and multiorgan apoptosis and dysfunction (evidenced by increased plasma levels of creatinine, blood urea nitrogen, alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase).


: Our results suggest that pre-existing inflammatory state may exacerbate the multiorgan injury during heat exposure. This tends to promote that pre-existing infection or sepsis may increase the risk of heatstroke.

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