Cecal ligation and puncture accelerates development of ventilator-induced XXXX .

@entity32 @entity295 @entity55 @entity4 @entity651 @entity1588 @entity2507 @entity1576 @entity3426 @entity35
@entity295 is a leading cause of @entity1576 requiring mechanical ventilation, but the interaction between @entity295 and ventilation is unclear. While prior studies demonstrated a priming role with endotoxin, actual septic animal models have yielded conflicting results regarding the role of preceding @entity295 on development of subsequent ventilator-induced @entity651 (VILI). Using a @entity35 @entity1588 ( @entity1588 ) model of @entity295 and subsequent injurious ventilation, we sought to determine if @entity295 affects development of VILI. Adult male @entity35 were subject to @entity1588 or sham operation and, after 12 h, underwent injurious mechanical ventilation (tidal volume 30 ml/kg, positive end-expiratory pressure 0 cm @entity2507 ) for either 0, 60, or 120 min. Biochemical and physiological measurements, as well as computed tomography, were used to assess injury at 0, 60, and 120 min of ventilation. Before ventilation, @entity1588 @entity35 had higher levels of alveolar neutrophils and @entity3426 . After 60 min of ventilation, @entity1588 @entity35 had worse injury as evidenced by @entity32 , permeability, respiratory static compliance, @entity4 , oxygenation, and computed tomography. By 120 min, @entity1588 and sham @entity35 had comparable levels of @entity651 as assessed by many, but not all, of these metrics. @entity1588 @entity35 had an accelerated and worse loss of end-expiratory lung volume relative to sham, and consistently higher levels of alveolar @entity3426 . Loss of aeration and progression of @entity4 was more pronounced in dependent lung regions. We conclude that @entity1588 @entity55 in @entity35 , and accelerated the development of subsequent VILI.
