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Updated: Jun 24, 2026
Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents
Published on: December 5, 2025
Pre-existing lipopolysaccharide may increase the risk of heatstroke in rats
Xiao-Jing Lin1, Ya-Jie Li, Zhi-Liang Li
1Department of Nursing, Nanfang Hospital, Southern University, Guangzhou, Guangdong, China.
Background:
: We attempted to ascertain whether pre-existing inflammatory state [caused by exogenous administration of lipopolysaccharide (LPS)] exacerbated multiorgan dysfunction in experimental heatstroke.
Design:
: 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.
Results:
: 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).
Conclusion:
: 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.
