A reversible model of acute lung injury based on ozone exposure.

In this study inflammatory responses were determined in rat lungs 0, 1, 3, and 8 days following single 2- and 4-hr exposures to 1.8 ppm ozone. Analysis of lavage fluid immediately following exposure demonstrated enhanced lactate dehydrogenase activity and decreased numbers of lavageable macrophages but no alterations in albumin content. Similar analyses at one day postexposure demonstrated 282% and 456% increases in albumin content and enhanced numbers of lavageable neutrophils from a control value of 0.01 +/- 0.01 to 0.27 +/- 0.10 and 0.78 +/- 0.11 million cells per lung for 2-hr and 4-hr exposures, respectively. The observed increased levels of albumin were also present at 3 days, at which time the number of lavageable neutrophils was not significantly different than control. At both one and 3 days postexposure, lavageable lymphocytes were significantly increased 10-fold from a control value of 0.03 +/- 0.01 million cells per lung. However, the number of lavageable macrophages was unaltered on day 1, but enhanced on day 3, giving values of 0.67 +/- 0.05 (control), 2.25 +/- 0.46 (2 hr), and 2.70 +/- 1.05 (4 hr) million cells per lung. By 8 days both inflammatory cell numbers and albumin levels had returned to control values. Since these data demonstrated different time courses for each inflammatory cell type, this reversible model of acute lung injury should be useful for establishing possible involvement of these cells in processes of lung injury.

Water deprivation and food restriction on pulmonary bacterial defenses in mice.

Mice deprived of water for 48 hr, mice allowed water but restricted in food intake to equal that consumed by the water-deprived mice, and control mice were exposed for 30 min to an aerosol of Serratia marcescens. Comparison of the number of organisms in the lungs of mice killed immediately after infection and those killed 4 hr later showed a normal reduction over the 4-hr period in the control mice. A significant increase, however, was observed in the water-deprived mice and an even greater increase in the food-restricted mice allowed water. The results did not correlate directly with the lung weight or lung water content. This reduction in bacterial defense could not be assigned solely to either water or food restriction.