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Am J Physiol Lung Cell Mol Physiol 279: L342-L349, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 2, L342-L349, August 2000

Determinants of surfactant function in acute lung injury and early recovery

R. Mora1,2, S. Arold3, Y. Marzan1, B. Suki3, and E. P. Ingenito1

1 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, and 2 Division of Pulmonary and Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston 02115; and 3 Department of Biomedical Engineering, Boston University, Boston, Massachusetts 02215

Relationships between lung function and surfactant function and composition were examined during the evolution of acute lung injury in guinea pigs. Lung mechanics and gas exchange were assessed 12, 24, or 48 h after exposure to nebulized lipopolysaccharide (LPS). Bronchoalveolar lavage (BAL) fluid was processed for phospholipid and protein contents and surfactant protein (SP) A and SP-B levels; surfactant function was measured by pulsating bubble surfactometry. Lung elastance, tissue resistance, and arterial-alveolar gradient were moderately elevated by 12 h after LPS exposure and continued to increase over the first 24 h but began to recover between 24 and 48 h. Similarly, the absolute amount of 30,000 g pelleted SP-A and SP-B, the phospholipid content of BAL fluid, and surfactant function declined over the first 24 h after exposure, with recovery between 24 and 48 h. BAL fluid total protein content increased steadily over the first 48 h after LPS nebulization. In this model of acute lung injury, the intra-alveolar repletion of surfactant components in early recovery led to improved surfactant function despite the presence of potentially inhibitory plasma proteins.

acute respiratory distress syndrome; lipopolysaccharide; apoprotein; pulsating bubble surfactometry; optimal ventilator waveform


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