Nonetheless, protein leakage, indicating increased microvascular permeability, another hallmark of VILI, was highest in those low V T groups that developed atelectasis due to lacking adequate RM (noRM, RM60) (Fig. 4) . Collapse of lung units is accompanied by an increase in vascular filtration pressure, leading to edema formation, when vascular barrier functions are impaired [43] . This is in line with the observed alveolar septal thickening. Furthermore, microvascular leakage may also interfere with pulmonary surfactant, thus contributing to a reduction of compliance [44] , which was clearly present in this model. Finally, in atelectatic lungs shear forces between closed and open alveoli may develop [1] . Taken together we conclude that a lack of recruitment manoeuvres may cause what has been termed atelectotrauma.