BIOCHEMICAL DETECTION OF TYPE-I CELL-DAMAGE AFTER NITROGEN DIOXIDE-INDUCED LUNG INJURY IN RATS

The first objective of the present study was to evaluate the utility o f rTI(40) in the assessment of alveolar injury in a model of milder ac ute lung injury. Rats were exposed to 18 parts/million NO2 for 12 h; c ontrol rats received filtered air for 12 h. In NO2-exposed rats, the t otal amount of rTI(40) in bronchoalveolar fluid was elevated a-fold co mpared with control values (P < 0.001); protein concentration was 8.5- fold of control values (P < 0.001). The increase in rTI(40) was associ ated with morphological evidence of injury to type I cells Limited to the proximal alveolar regions of the lung. The second objective was to correlate the severity of alveolar type I cell injury with functional measurements of lung epithelial barrier integrity. NO2 inhalation sti mulated distal air space fluid clearance despite a significant increas e in lung endothelial and epithelial permeability to protein. These da ta demonstrate that rTI(40) is a useful biochemical marker for mild fo cal injury and that exposure to NO2 alters lung barrier function. Take n together with our earlier studies, these results suggest that the qu antity of recoverable rTI(40) can be used as an index of the severity of damage to the alveolar epithelium.