title: Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung.
abstract: BACKGROUND
  Septic shock is often associated with acute respiratory distress syndrome, a serious clinical problem exacerbated by improper mechanical ventilation. Ventilator-induced lung injury (VILI) can exacerbate the lung injury caused by acute respiratory distress syndrome, significantly increasing the morbidity and mortality. In this study, we asked the following questions: what is the effect of the lung position (dependent lung versus nondependent lung) on the rate at which VILI occurs in the normal lung? Will positive end-expiratory pressure (PEEP) slow the progression of lung injury in either the dependent lung or the nondependent lung?
  
  
  METHODS
  Sprague-Dawley rats (n = 19) were placed on mechanical ventilation, and the subpleural alveolar mechanics were measured with an in vivo microscope. Animals were placed in the lateral decubitus position, left lung up to measure nondependent alveolar mechanics and left lung down to film dependent alveolar mechanics. Animals were ventilated with a high peak inspiratory pressure of 45 cmH2O and either a low PEEP of 3 cmH2O or a high PEEP of 10 cmH2O for 90 minutes. Animals were separated into four groups based on the lung position and the amount of PEEP: Group I, dependent + low PEEP (n = 5); Group II, nondependent + low PEEP (n = 4); Group III, dependent + high PEEP (n = 5); and Group IV, nondependent + high PEEP (n = 5). Hemodynamic and lung function parameters were recorded concomitant with the filming of alveolar mechanics. Histological assessment was performed at necropsy to determine the presence of lung edema.
  
  
  RESULTS
  VILI occurred earliest (60 min) in Group II. Alveolar instability eventually developed in Groups I and II at 75 minutes. Alveoli in both the high PEEP groups were stable for the entire experiment. There were no significant differences in arterial PO2 or in the degree of edema measured histologically among experimental groups.
  
  
  CONCLUSIONS
  This open-chest animal model demonstrates that the position of the normal lung (dependent or nondependent) plays a role on the rate of VILI.
authors: Upstate Medical University, Department of Surgery, 750 E Adams Street, Syracuse, NY 13210 USA.
authors: Lucio
authors: L
authors: Pavone
authors: Scott
authors: S
authors: Albert
authors: Joseph
authors: J
authors: DiRocco
authors: Louis
authors: L
authors: Gatto
authors: Gary
authors: G
authors: Nieman
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D011650:Pulmonary Alveoli / Q000293:injuries* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012121:Respiration, Artificial / Q000009:adverse effects*; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D012129:Respiratory Function Tests