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Unilateral Acid Aspiration Augments the Effects of Ventilator Lung Injury in the Contralateral Lung
- Publication Year :
- 2013
-
Abstract
- 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 (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. RESULTS:: 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. 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 VT.
Details
- Database :
- OAIster
- Notes :
- English
- Publication Type :
- Electronic Resource
- Accession number :
- edsoai.on1308905256
- Document Type :
- Electronic Resource