Unilateral acid aspiration augments the effects of ventilator lung injury in the contralateral lung.

Abstract

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. Mice, instilled with hydrochloric acid (HCl) in the right lung, was assigned to one of the following groups: mechanical ventilation with tidal volumes (VT) 25 ml/kg (HCl-VILI25, n = 12), or VT 15 ml/kg (HCl-VILI15, n = 9), or spontaneous breathing (HCl-SB, n = 14). Healthy mice were ventilated with VT 25 ml/kg (VILI25, n = 11). Arterial oxygenation, lung compliance, bronchoalveolar lavage inflammatory cells, albumin, and cytokines concentration were measured. After 7 h, 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 µl/cm H2O, mean ± SD, respectively). After right lung injury, the left lung of HCl-VILI25 group received a greater fraction of the VT than the VILI25 group, despite an identical global VT. 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 µg/ml; P < 0.05). Cytokines levels did not differ between groups. 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 VT.