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1 Department of Medicine, Vermont Lung Center, University of Vermont, Burlington, VT, USA; Pulmonary/Critical Care, Fletcher Allen Health Care, Burlington, VT, USA
2 Department of Medicine, Vermont Lung Center, University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: gil.allen{at}uvm.edu.
In a previous study (Allen et al. J Appl Physiol 93:1709-1715, 2002) we used deep inflations (DI) in mice to show that recruitment of closed lung units can be a very transient phenomenon in lung injury. The purpose of this study was to investigate how this transience of lung recruitment depends on the nature and degree of acute lung injury (ALI). Mice were administered 50µl of either saline (n=8), 0.01M (n=9) or 0.025M (n=8) hydrochloric acid, or 50 µg (n=10) or 150µg (n=6) of lipopolysaccharide (LPS) and mechanically ventilated 24 to 48 hours later. At various levels of positive end-expiratory pressure (PEEP), 2 DIs were delivered, and forced-oscillations were used to obtain a measure of lung stiffness (H) periodically over 7 min. Following LPS exposure, pressure-volume (PV) curve hysteresis and recovery in HM following DI were no different from saline-exposed controls despite 500 times more neutrophils in bronchoalveolar lavage fluid (BALF). PV hysteresis and recovery in H were increased in acid-exposed mice (<0.001), and correlated with BALF protein content (R= 0.81). PEEP reduced recovery in H in all groups (p<0.01) but reduced PV hysteresis in the acid-injured groups only (p<0.001). We conclude that the effects of DI's in ALI depend on the degree of lung injury, but only to the extent that this injury reflects a disruption of the air-liquid interface.
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