title: Low tidal volume protects pulmonary vasomotor function from "second-hit" injury in acute lung injury rats.
abstract: 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.
authors.affiliation: Department of Critical Care Medicine, Zhongda Hospital, Southeast University Medical School, Nanjing, Jiangsu, China.
authors.forename: Chun
authors.initials: C
authors.lastname: Pan
authors.forename: Jianqiang
authors.initials: J
authors.lastname: Wang
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.forename: Ling
authors.initials: L
authors.lastname: Liu
authors.forename: Liang
authors.initials: L
authors.lastname: Jing
authors.forename: Yi
authors.initials: Y
authors.lastname: Yang
authors.forename: Haibo
authors.initials: H
authors.lastname: Qiu
mesh_terms: D055371:Acute Lung Injury / Q000503:physiopathology*; D000818:Animals; D008168:Lung / Q000503:physiopathology*; D011651:Pulmonary Artery / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012008:Recurrence; D013990:Tidal Volume; D014666:Vasomotor System / Q000503:physiopathology*