A pressure of 30 cmH 2 O for each RM was necessary to maintain lung volume stable. In accordance with previous studies [4, 5] RM with 25 cmH 2 O peak pressure were not sufficient to avoid a loss of lung volume (data not shown). The double sigmoidal nature of the murine pressure volume curve [38] may explain the positive response to RM with 30 cmH 2 O pressure. According to Zosky et al. [38] , pressures above 20 cmH 2 O induce fundamental changes in the murine lung, resulting in increased compliance. These changes are proposed to be either due to reopening of collapsed alveoli or to a secondary population of alveoli that are present but not aerated below a critical transrespiratory pressure [39] . In the present study, measurement of lung input impedance revealed that the alterations in pulmonary resistance and compliance in RM60 and noRM mice were predominantly due to changes in the periphery of the lung. Although we observed significant differences in R aw between RM5, RM60 and noRM mice ventilated at the same V T , this effect was rather small, indicating that bronchoconstriction of large airways is of minor importance to explain our findings. The strong increase in G and H in mice ventilated without RM demonstrates a progressive loss in lung volume [24] . Increases in tissue damping reflect energy dissipation and are associated with an increase in tissue resistance and/or regional heterogeneity as result of peripheral airway constriction, whereas tissue elastance reflects energy storage in lung tissues and represents lung stiffness [5] . The small decrease in hysteresivity shows that H increased slightly stronger than G. Further, it underlines that impaired lung functions were not primarily due to heterogeneity caused by narrowing of small airways [40] . Thus narrowing of conductive airways played only a minor role in this model and we conclude that the loss of lung volume was mainly due to formation of atelectasis.