Experimental ventilator-induced lung injury (VILI) is characterized by alterations in alveolar epithelial and microvascular permeability that favors the systemic dissemination of lung borne cytokines or bacteria. Animal models of VILI have been shown relevant to patient care and outcome and help explaining why most patients with the acute respiratory distress syndrome do not die from respiratory failure but from multiple organ dysfunction. Recent experimental studies also showed that adverse ventilator patterns may propel airway secretions and bacteria to previously healthy lung regions. Noninvasive imaging techniques were used for years to study the net rate of protein flow across the pulmonary microvascular endothelium and the alveolar epithelium in vivo, during normal breathing and lung inflation. More recently, the two-way protein fluxes across the alveolo-capillary barrier and the intra-pulmonary dispersion of alveolar edema have been monitored during mechanical ventilation. These experiments have provided new insights on the mechanisms of experimental VILI that may be of clinical value. This review will describe the evolution of these techniques and their main physiological and pharmacological applications in the era of VILI
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