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A Murine Model of Volutrauma*: Potential Contribution of Inflammatory Cell Proteases to Lung Injury

T. Gronski, Jr., MD, FCCP; E. Lum, MD; J. Campbell; S. D. Shapiro, MD, FCCP
Author and Funding Information

*From the Departments of Medicine and Cell Biology, Washington University School of Medicine, St. Louis, MO. Supported by ALA and the Barnes-Jewish Hospital Foundation.

Correspondence to: Theodore J. Gronski, Jr., MD, FCCP, Pulmonary and Critical Care Medicine, Barnes Jewish Hospital North, 216 S Kingshighway Blvd, St. Louis, MO 63110



Chest. 1999;116(suppl_1):28S. doi:10.1378/chest.116.suppl_1.28S
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Extract

Although mechanical ventilation is recognized as an invaluable method of support for patients with severe respiratory failure, recent attention has been drawn to the phenomenon of lung injury caused by positive pressure ventilation. Studies of the pathogenesis of “volutrauma” have focused largely on the mechanical sequelae of excessive or repetitive alveolar distention, eg, the “stretched pore” phenomenon or capillary stress fracture. Even early investigations into lung injury associated with mechanical ventilation, however, have identified inflammatory cell accumulation with increasing airway pressures. We have developed a closed-chest murine model of volutrauma to pursue the individual contributions of these two potential mechanisms of lung injury.


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