Alveolar permeability to protein in rats differentially susceptible to ozone.

Abstract

Sprague-Dawley rats susceptible (DS) to NaCl-induced hypertension suffer higher mortality when exposed daily to 2.0 ppm ozone than do hypertension-resistant (DR) rats, independent of salt in the diet or systemic blood pressure. To investigate one possible contribution to this differential sensitivity to ozone, alveolar permeabilities to serum albumin were measured both in ozone-exposed and in control DS and DR rats. Female rats aged 5-7 weeks maintained on a low-salt (0.4% NaCl) diet were injected intravenously with 125I-bovine serum albumin and were then exposed to either 2.0 ppm ozone or air for 5 h. After pentobarbital anesthesia, the rats were exsanguinated and their lungs were lavaged in situ with saline. Lavage fluids and blood samples were measured for radioactivity using a NaI-well gamma counter. The results indicated that while DS and DR control rats have similar pulmonary permeabilities to 125I-albumin, the lungs of the ozone-exposed DS animals were 63% (p less than 0.02) more permeable than those of DR rats exposed to ozone. Sloughing of epithelial tissue, mucous formation and an accumulation of macrophages in the end-airways were more pronounced among ozone-exposed DS animals than in DR-ozone-exposed rats. This increased damage among DS rats correlated well with the increased protein permeability levels. In similar studies, Sprague-Dawley (D) rats were more variable in their response to ozone than either inbred strain. However, the results appeared generally more like those of the DS animals, suggesting that the trait selected by inbreeding may have been resistance rather than sensitivity to ozone-induced lung injury.