Hyperoxia but not high tidal volume contributes to ventilator-induced lung injury in healthy mice

BMC Pulmonary Medicine

Research

Taiga Ichinomiya¹  Tetsuya Hara¹  Chiaki Inadomi¹  Yu Li²  Da Zhai³  Tao-Sheng Li³  Yong Xu³  Chen Yan³  Jingyan Liang⁴ 

[1] Department of Anesthesiology and Intensive Care Medicine, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, 852-8501, Nagasaki, Japan;Department of Anesthesiology, The Second Affiliated Hospital of Nanchang University, 330006, Nanchang City, Jiangxi Province, China;Department of Stem Cell Biology, Atomic Bomb Disease Institute, Nagasaki University, 1-12-4 Sakamoto, 852-8523, Nagasaki, Japan;Department of Stem Cell Biology, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, 852-8523, Nagasaki, Japan;Institute of Translational Medicine, Medical College, Yangzhou University, 225000, Yangzhou, Jiangsu, P.R. China;

关键词: Mechanical ventilation;    Tidal volume;    Oxidative damage;    Inflammatory response;    Mechanotransduction;   

DOI  :  10.1186/s12890-023-02626-x

 received in 2023-05-28, accepted in 2023-08-31,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundMechanical ventilation is a supportive therapy used to maintain respiratory function in several clinical and surgical cases but is always accompanied by lung injury risk due to improper treatment. We investigated how tidal volume and oxygen delivery would contribute independently or synergistically to ventilator-induced lung injury (VILI).MethodsUnder general anesthesia and tracheal intubation, healthy female C57BL/6 N mice (9 weeks old) were randomly ventilated for 2 h by standard (7 ml/kg) or high (14 ml/kg) tidal volume at positive end-expiratory pressure (PEEP) of 2 cmH2O, with room air, 50% O2 (moderate hyperoxia), or 100% O2 (severe hyperoxia); respectively. Mice were sacrificed 4 h after mechanical ventilation, and lung tissues were collected for experimental assessments on lung injury.ResultsCompared with the healthy control, severe hyperoxia ventilation by either standard or high tidal volume resulted in significantly higher wet-to-dry lung weight ratio and higher levels of IL-1β and 8-OHdG in the lungs. However, moderate hyperoxia ventilation, even by high tidal volume did not significantly increase the levels of IL-1β and 8-OHdG in the lungs. Western blot analysis showed that the expression of RhoA, ROCK1, MLC2, and p-MLC2 was not significantly induced in the ventilated lungs, even by high tidal volume at 2 cmH2O PEEP.ConclusionSevere hyperoxia ventilation causes inflammatory response and oxidative damage in mechanically ventilated lungs, while high tidal volume ventilation at a reasonable PEEP possibly does not cause VILI.

【 授权许可】

CC BY   
© BioMed Central Ltd., part of Springer Nature 2023

【 图 表 】

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Fig. 2