Low tidal volume protects pulmonary vasomotor function from “second-hit” injury in acute lung injury rats

Respiratory Research

Haibo Qiu³  Yi Yang³  Liang Jing⁴  Ling Liu³  Wei Liu¹  Jianqiang Wang²  Chun Pan³ 

[1] School of pharmacy, China Pharmaceutical University, Nanjing, Jiangsu, China;Department of Critical Care Medicine, Jintan Hospital, Changzhou, Jiangsu, China;Department of Critical Care Medicine, Zhongda Hospital, Southeast University Medical School, Nanjing, Jiangsu, China;Department of Anesthesiology, Zhongda Hospital, Southeast University, Nanjing, Jiangsu, China

关键词: Pulmonary hypertension;    Lung injury;    Vascular injury;    Vascular reactivity;    Mechanical ventilation;    Endothelium;   

Others  :  796660
DOI  :  10.1186/1465-9921-13-77

 received in 2012-04-03, accepted in 2012-08-24,  发布年份 2012

【 摘 要 】

Background

Sepsis could induce indirect acute lung injury(ALI), and pulmonary vasomotor dysfunction. While low tidal volume is advocated for treatment of ALI patients. However, there is no evidence for low tidal volume that it could mitigate pulmonary vasomotor dysfunction in indirect ALI. Our study is to evaluate whether low tidal volume ventilation could protect the pulmonary vascular function in indirect lipopolysaccharide (LPS) induced acute lung injury rats.

Methods

An indirect ALI rat model was induced by intravenous infusion of LPS. Thirty rats (n = 6 in each group) were randomly divided into (1)Control group; (2) ALI group; (3) LV group (tidal volume of 6mL/kg); (4) MV group (tidal volume of 12mL/kg); (5)VLV group (tidal volume of 3mL/kg). Mean arterial pressure and blood gas analysis were monitored every 2 hours throughout the experiment. Lung tissues and pulmonary artery rings were immediately harvested after the rats were bled to be killed to detect the contents of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS) and TNF-α. Acetylcholine (Ache)-induced endothelium-dependent and sodium nitroprusside (SNP)-induced endothelium-independent relaxation of isolated pulmonary artery rings were measured by tensiometry.

Results

There was no difference within groups concerning blood pressure, PaCO₂ and SNP-induced endothelium-independent relaxation of pulmonary artery rings. Compared with MV group, LV group significantly reduced LPS-induced expression of ET-1 level (113.79 ± 7.33pg/mL vs. 152.52 ± 12.75pg/mL, P < 0.05) and TNF-α (3305.09 ± 334.29pg/mL vs.4144.07 ± 608.21pg/mL, P < 0.05), increased the expression of eNOS (IOD: 15032.05 ± 5925.07 vs. 11454.32 ± 6035.47, P < 0.05). While Ache (10^-7mol/L-10^-4mol/L)-induced vasodilatation was ameliorated 30% more in LV group than in MV group.

Conclusions

Low tidal volume could protect the pulmonary vasodilative function during indirect ALI by decreasing vasoconstrictor factors, increasing expressions of vasodilator factors in pulmonary endothelial cells, and inhibiting inflammation injuries.

【 授权许可】

   
2012 Pan et al.; licensee BioMed Central Ltd.

【 图 表 】

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