Many experimental models have been designed to explore how ventilation could damage lungs and produce permeability-type pulmonary edema. Edema produced by ventilation with a high tidal volume varies in severity depending on the intensity and duration of the challenge and on previous lung state. Alveolar flooding with foam in airways excludes zones from the ventilation, and creates a vicious circle that increases the risk of overinflation of the remaining ventilated areas. This risk exists in patients suffering from the acute respiratory distress syndrome, even if ventilated with low tidal volumes. It is thus important to recruit zones filled with edematous liquid, and a means to achieve this goal is to accelerate alveolar liquid absorption. This may be obtained by activation of molecular mechanisms implicated in vectorial sodium transport by alveolar-bronchiolar cells responsible for liquid absorption, such as the sodium channel or the Na,K-ATPase pump. Unfortunately, overinflation experimentally decreases alveolar liquid resorption by depressing Na,K-ATPase function in the alveolar epithelium (1), for a yet unclear reason. Normal absorption may be restored in rat lungs submitted to overinflation by stimulating sodium transport with -adrenergic agonists (2), although these agents have not proven as effective in a similar model (3) or in patients with acute lung injury (4).