Further evidence for the formation of atelectasis was given by blood gas analysis, which revealed impaired gas exchange in lowV T noRM and lowV T RM60 mice (Fig. 3 , Table 3 ). The present study demonstrates that impairment of gas exchange, to a level that would fulfil the clinical definition for ARDS [42] , can be caused by a ventilation strategy that leads to derecruitment of lung volume. On the other hand, our data on lung histopathology, neutrophil count and BAL levels of pro-inflammatory cytokines indicate that inflammatory lung injury was not severe even in the lowV T noRM group. Notably, neutrophil counts and histopathological alterations ( Fig. 6-8 ) did not correlate well with gas exchange and lung functions, further supporting our conclusion that atelectasis rather than inflammation was the major reason for the impaired gas exchange in the groups ventilated without sufficient RM. In fact, neutrophil infiltration was highest in the high V T groups, suggesting ventilation-induced inflammation (biotrauma) as a mechanism.