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1Department of Medicine, Vermont Lung Center, University of Vermont, Burlington; 2Fletcher Allen Health Care, Burlington, Vermont; and 3Department of Surgery, State University of New York Upstate Medical University, Syracuse, New York
Submitted 1 December 2004 ; accepted in final form 11 April 2005
The mechanical derangements in the acutely injured lung have long been ascribed, in large part, to altered mechanical function at the alveolar level. This has not been directly demonstrated, however, so we investigated the issue in a rat model of overinflation injury. After thoracotomy, rats were mechanically ventilated with either 1) high tidal volume (VT) or 2) low VT with periodic deep inflations (DIs). Forced oscillations were used to measure pulmonary impedance every minute, from which elastance (H) and hysteresivity (
) were derived. Subpleural alveoli were imaged every 15 min using in vivo video microscopy. Cross-sectional areas of individual alveoli were measured at peak inspiration and end exhalation, and the percent change was used as an index of alveolar instability (%I-E
). Low VT never led to an increase in %I-E
but did result in progressive atelectasis that coincided with an increase in H but not
. DI reversed atelectasis due to low VT, returning H to baseline. %I-E
, H, and
all began to rise by 30 min of high VT and were not reduced by DI. We conclude that simultaneous increases in both H and
are reflective of lung injury in the form of alveolar instability, whereas an isolated and reversible increase in H during low VT reflects merely derecruitment of alveoli.
ventilator-induced lung injury; acute respiratory distress syndrome; in vivo microscopy; alveolar recruitment; respiratory mechanics
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