High driving pressure ventilation induces pulmonary hypertension in a rabbit model of acute lung injury

作者：Yonghao Xu, Yu Zhang, Jie Zhang, Weibo Liang, Ya Wang, Zitao Zeng, Zhenting Liang, Zhaoyi Ling, Yubiao Chen, Xiu-Mei Deng, Yongbo Huang, Xiaoqing Liu, Haibo Zhang, Yimin Li · 发表于：Journal of Intensive Care · 年份：2023 · DOI：10.1186/s40560-023-00689-w · 被引用次数：6 · 研究领域：Chronic Obstructive Pulmonary Disease (COPD) Research、Ferroptosis and cancer prognosis、Inflammation biomarkers and pathways

Abstract Background Mechanical ventilation may cause pulmonary hypertension in patients with acute lung injury (ALI), but the underlying mechanism remains elucidated. Methods ALI was induced in rabbits by a two-hit injury, i.e., hydrochloric acid aspiration followed by mechanical ventilation for 1 h. Rabbits were then ventilated with driving pressure of 10, 15, 20, or 25 cmH 2 O for 7 h. Clinicopathological parameters were measured at baseline and different timepoints of ventilation. RNA sequencing was conducted to identify the differentially expressed genes in high driving pressure ventilated lung tissue. Results The two-hit injury induced ALI in rabbits was evidenced by dramatically decreased PaO 2 /FiO 2 in the ALI group compared with that in the control group (144.5 ± 23.8 mmHg vs. 391.6 ± 26.6 mmHg, P < 0.001). High driving pressure ventilation (20 and 25 cmH 2 O) significantly elevated the parameters of acute pulmonary hypertension at different timepoints compared with low driving pressure (10 and 15 cmH 2 O), along with significant increases in lung wet/dry ratios, total protein contents in bronchoalveolar lavage fluid, and lung injury scores. The high driving pressure groups showed more pronounced histopathological abnormalities in the lung compared with the low driving pressure groups, accompanied by significant increases in the cross-sectional areas of myocytes, right ventricular weight/body weight value, and Fulton’s index. Furthermore, the expression of the gen...