Background: Mechanical ventilation is necessary during acute respiratory distress syndrome, but it promotes lung injury because of the excessive stretch applied to the aerated parenchyma. The authors' hypothesis was that after a regional lung injury, the noxious effect of mechanical ventilation on the remaining aerated parenchyma would be more pronounced. Methods: Mice, instilled with hydrochloric acid (HCl) in the right lung, was assigned to one of the following groups: mechanical ventilation with tidal volumes (V-T) 25ml/kg (HCl-VILI25, n = 12), or V-T 15ml/kg (HCl-VILI15, n = 9), or spontaneous breathing (HCl-SB, n = 14). Healthy mice were ventilated with V-T 25ml/kg (VILI25, n = 11). Arterial oxygenation, lung compliance, bronchoalveolar lavage inflammatory cells, albumin, and cytokines concentration were measured. Results: After 7h, oxygenation and lung compliance resulted lower in HCl-VILI25 than in VILI25 (P < 0.05, 210 +/- 54 vs. 479 +/- 83 mmHg, and 32 +/- 3.5 vs. 45 +/- 4.1 mu l/cm H2O, mean +/- SD, respectively). After right lung injury, the left lung of HCl-VILI25 group received a greater fraction of the V-T than the VILI25 group, despite an identical global V-T. The number of total and polymorphonuclear cells in bronchoalveolar lavage resulted significantly higher in HCl-VILI25, compared with the other groups, in not only the right lung, but also in the left lung. The albumin content in the left lung resulted higher in HCl-VILI25 than in VILI25 (224 +/- 85 vs. 33 +/- 6 mu g/ml; P < 0.05). Cytokines levels did not differ between groups. Conclusion: Aggressive mechanical ventilation aggravates the preexisting lung injury, which is noxious for the contralateral, not previously injured lung, possibly because of a regional redistribution of V-T.
