title: Higher frequency ventilation attenuates lung injury during high-frequency oscillatory ventilation in sheep models of acute respiratory distress syndrome.
abstract: BACKGROUND
  High-frequency oscillatory ventilation (HFOV) at higher frequencies minimizes the tidal volume. However, whether increased frequencies during HFOV can reduce ventilator-induced lung injury remains unknown.
  
  
  METHODS
  After the induction of acute respiratory distress syndrome in the model by repeated lavages, 24 adult sheep were randomly divided into four groups (n = 6): three HFOV groups (3, 6, and 9 Hz) and one conventional mechanical ventilation (CMV) group. Standard lung recruitments were performed in all groups until optimal alveolar recruitment was reached. After lung recruitment, the optimal mean airway pressure or positive end-expiratory pressure was determined with decremental pressure titration, 2 cm H2O every 10 min. Animals were ventilated for 4 h.
  
  
  RESULTS
  After lung recruitment, sustained improvements in gas exchange and compliance were observed in all groups. Compared with the HFOV-3 Hz and CMV groups, the transpulmonary pressure and tidal volumes were statistically significantly lower in the HFOV-9 Hz group. The lung injury scores and wet/dry weight ratios were significantly reduced in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Expression of interleukin-1β and interleukin-6 in the lung tissue, decreased significantly in the HFOV-9 Hz group compared with the HFOV-3 Hz and CMV groups. Malondialdehyde expression and myeloperoxidase activity in lung tissues in the HFOV-9 Hz group decreased significantly, compared with the HFOV-3 Hz and CMV groups.
  
  
  CONCLUSIONS
  The use of HFOV at 9 Hz minimizes lung stress and tidal volumes, resulting in less lung injury and reduced levels of inflammatory mediators compared with the HFOV-3 Hz and CMV conditions.
authors.affiliation: Department of Critical Care Medicine, Nanjing Zhongda Hospital, School of Medical, Southeast University, Nanjing, Jiangsu, PR China.
authors.forename: Songqiao
authors.initials: S
authors.lastname: Liu
authors.forename: Yang
authors.initials: Y
authors.lastname: Yi
authors.forename: Maohua
authors.initials: M
authors.lastname: Wang
authors.forename: Qiuhua
authors.initials: Q
authors.lastname: Chen
authors.forename: Yingzi
authors.initials: Y
authors.lastname: Huang
authors.forename: Ling
authors.initials: L
authors.lastname: Liu
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Xie
authors.forename: Dunyuan
authors.initials: D
authors.lastname: Zhou
authors.forename: Haibo
authors.initials: H
authors.lastname: Qiu
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006612:High-Frequency Ventilation / Q000379:methods*; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D009195:Peroxidase / Q000097:blood; D011175:Positive-Pressure Respiration / Q000379:methods; D012121:Respiration, Artificial / Q000379:methods; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000628:therapy*; D012756:Sheep; D013990:Tidal Volume; D055397:Ventilator-Induced Lung Injury / Q000097:blood / Q000517:prevention & control*
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D008315:Malondialdehyde; D009195:Peroxidase