In normal rabbits subjected to saline lavage, injurious mechanical ventilation was shown to significantly increase lung neutrophil accumulation and chemi- luminescence (an indicator of neutrophil priming) (11, 12), as well as bronchoalveolar lavage (BAL) levels of inflammatory mediators (platelet activating factor and thromboxane-B 2 [13]) and expression of tumor necrosis factor-alpha (TNF- a ) by al- veolar macrophages (14). Similarly, in rat lungs ventilated ex vivo increased BAL concentrations of a number of cytokines (including TNF-
a
and interleukin-1
b
[IL-1
b
]) were found fol- lowing injurious mechanical ventilation with low end-expiratory lung volumes allowing tidal alveolar reopening and collapse with each breath (15). The superimposition of high end-inspira- tory lung volume (i.e., large tidal volume) on low end-expira- tory lung volume leads to a further synergistic increase in BAL cytokine concentrations (15).