title: Molecular mechanism of sustained inflation in acute respiratory distress syndrome.
abstract: BACKGROUND
  The aim of this study was to investigate the effect and the potential molecular mechanism of sustained inflation (SI) recruitment maneuvers in acute respiratory distress syndrome (ARDS) in beagle dog following endotracheal suctioning.
  
  
  METHODS
  ARDS was induced in 24 beagle dogs with oleic acid. They had mechanical ventilation support. They were randomized into four groups after the establishment of the ARDS model: non-SI-open group where no SI was applied in beagle dogs with ARDS following open endotracheal suctioning; non-SI-closed group where no SI was applied in beagle dogs with ARDS following closed endotracheal suctioning; SI-open group where SI was applied in beagle dogs with ARDS following open endotracheal suctioning; and SI-closed group where SI was applied in beagle dogs with ARDS following closed endotracheal suctioning. Oxygenation, indexes of respiratory mechanics, and hemodynamic indexes were serially measured during the procedure. The serum protein level, or the messenger RNA in the heart and lung, of inflammation-related cytokines was investigated.
  
  
  RESULTS
  SI in ARDS improved oxygenation, lung compliance, and airway resistance but had no significant effect in the hemodynamic indexes. At molecular level, SI in ARDS neutralized the increases of pro-inflammatory cytokines (tumor necrosis factor α, interleukin 1β [IL-1β], and IL-6), and anti-inflammatory cytokine (IL-10) in the serum. Furthermore, SI in ARDS increased aquaporin 1 and aquaporin 5 messenger RNA in the lung tissue, and decreased IL-6 messenger RNA in the lung and heart tissue.
  
  
  CONCLUSIONS
  SI in ARDS could improve oxygenation, lung compliance, and airway resistance, which was related to the improved degree of inflammation and better maintained aquaporins.
authors.affiliation: Department of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhao
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Yong
authors.initials: Y
authors.lastname: Fang
authors.forename: Xiantao
authors.initials: X
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Shen
authors.forename: Tongwa
authors.initials: T
authors.lastname: Cao
authors.forename: Hechen
authors.initials: H
authors.lastname: Zhu
mesh_terms: D000403:Airway Resistance / Q000502:physiology; D000818:Animals; D020346:Aquaporins / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D004285:Dogs; D018836:Inflammation Mediators / Q000378:metabolism; D007442:Intubation, Intratracheal; D008170:Lung Compliance / Q000502:physiology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D011175:Positive-Pressure Respiration / Q000379:methods*; D012333:RNA, Messenger / Q000378:metabolism; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000378:metabolism* / Q000628:therapy*; D015656:Respiratory Mechanics / Q000502:physiology; D013396:Suction
chemical_list: D020346:Aquaporins; D016207:Cytokines; D018836:Inflammation Mediators; D012333:RNA, Messenger