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1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, Fletcher Allen Health Care, University of Vermont, Burlington, VT, USA; Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA
2 Department of Anesthesia, University of California, San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA; Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
3 Division of Pulmonary and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA
4 Department of Anesthesia, University of California, San Francisco, San Francisco, CA, USA; Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: polly.parsons{at}vtmednet.org.
Ventilator induced lung injury (VILI) is an inflammatory
process that can be attenuated by lung protective
ventilation strategies. This study had three objectives to
further investigate the pathogenesis of acute lung injury
(ALI) and VILI and the mechanism of lung protection in
these syndromes: 1) to determine if plasma measurements of
soluble tumor necrosis factor receptor I (sTNFRI) and II
(sTNFRII) would predict the development of ALI and
mortality in a small single center trial; 2) To test the
predictive value of these markers and of tumor necrosis
factor (TNF-
) in a larger, broader group of patients with ALI; 3) To test the hypothesis that low tidal volume ventilation would be associated with a decrease in plasma levels of TNF-, sTNFRI and sTNFRII. In the single center study, sTNFRI and II levels were higher in patients at risk for and with ALI but they did not predict the development of the syndrome. In the multicenter trial sTNFRI and II were strongly associated with mortality (OR 5.76 per 1 log10 increment in receptor level; 95% CI 2.63 to 12.6 and OR 2.58; 95% CI 1.05 to 6.31, respectively) and morbidity measured as fewer non-pulmonary organ failure free days and fewer ventilator free days. The low tidal volume ventilation strategy was associated with an attenuation of plasma sTNFRI levels (p=0.037). In vitro, stimulated A549 cells release sTNFRI but not sTNRFII. In conclusion, plasma levels of sTNFRI and II can serve as biomarkers for morbidity and mortality in patients with ALI. Furthermore, low tidal volume ventilation is associated with a specific decrease in sTNFRI levels. This suggests that one beneficial effect of low tidal volume ventilation may be to attenuate alveolar epithelial injury.
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