Related Experiment Video
Updated: Aug 9, 2026
Non-Invasive Endotracheal Administration of Lipopolysaccharide to Induce Acute Lung Injury in Rodents
Published on: December 5, 2025
[Arterial blood gas analysis in Lipopolysaccharide-heat co-stressed rats]
Xiao-jing Lin1, Bing-de Luo, Ya-jie Li
1Southern Hospital, Southern Medical University, Guangzhou 510515, China.
Objective:
To observe the change in vital signs and arterial blood gas in Lipopolysaccharide (LPS)-injected heat exposed rats.
Methods:
Male pathogen-free Wistar rats were randomly assigned to the following groups: saline-injected normothermic control (C-Group), saline-injected heat exposed (H-Group), LPS-injected normothermic control (L-Group), LPS-injected heat exposed (HL-Group). Rectal temperature (Tr), heart rate (HR), mean arterial pressure (MAP), arterial blood gas were continually monitored.
Results:
(1) The rats in HL-Group displayed significantly high values of Tr (43.04 degrees C +/- 0.11 degrees C) and HR [(660 +/- 42) beats/min] and low values of MAP [(49.0 +/- 3.5) mm Hg] compared with C-Group. There was a significant difference in the values of Tr, HR, and MAP between HL-Group and L-Group and in the values of HR and MAP between HL-Group and H-Group. (2) The values of PaO(2), HCO(3)(-), PaCO(2) were significantly lower than those in C-Group at 40 min after LPS-injected heat stress. At 120 min, the PaO(2) [(11.59 +/- 1.11) kPa], HCO(3)(-) [(10.42 +/- 1.06) mmol/L], PaCO(2) [(2.82 +/- 0.81) kPa] in HL-Group were significantly lower than those in L-Group. A significant difference in the values of HCO(3)(-) and PaCO(2) between HL-Group and H-Group was also observed.
Conclusion:
LPS-injected heat stress primes the rat to advance and augment the change in vital signs, arterial blood gas, and systemic inflammatory response syndrome.
