Journal
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
Volume 165, Issue 2, Pages 242-249Publisher
AMER THORACIC SOC
DOI: 10.1164/ajrccm.165.2.2108087
Keywords
acute respiratory distress syndrome; alveolar type I cell antigen; von Willebrand factor antigen; respiration; artificial adverse effects; alveolar fluid clearance
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Funding
- NHLBI NIH HHS [HL 04372, HL 51854, K08 HL069900-02, R56 HL088440, K08 HL069900] Funding Source: Medline
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Using a rat model of acid-induced lung injury, we tested the hypothesis that tidal volume reduction at the same level of PEEP (10 cm H2O) would diminish the degree of pulmonary edema by attenuating injury to the alveolar epithelial and endothelial barriers. Tidal volume reduction from 12 to 6 to 3 ml/kg significantly reduced the rate of lung water accumulation from 690 mul/h to 310 mul/h to 210 mul/h. Ventilation with either 6 or 3 ml/kg reduced endothelial injury equally as measured by plasma vWf:Ag and permeability to albumin. Plasma RTI40, a marker of type I epithelial cell injury, decreased 46% when tidal volume was reduced from 12 to 6 ml/kg and decreased an additional 33% with 3 ml/kg (p < 0.05). The rate of alveolar epithelial fluid clearance was significantly faster in the 3-ml/kg group (24 +/- 7%/h) compared with 6 ml/kg (115 +/- 11%/h) and 112 ml/kg (3 +/- 6%/h). We conclude that low tidal volume ventilation protects both the alveolar epithelium and the endothelium in this model of acute lung injury. The additional decrease in pulmonary edema with a tidal volume of 3 ml/kg is partly accounted for by greater protection of, the alveolar epithelium.
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