BREATHING AND PULMONARY SURFACTANT FUNCTION IN MICE 24 H AFTER OZONE EXPOSURE

The aim of this study was to determine whether an acute ozone exposure affects breathing, and the ability. of pulmonary surfactant to mainta in the patency of terminal conducting airways, BALB/c mice were expose d to ozone (1 part per million (ppm)) for 2, 4, 6, and 8 h, They were examined with plethysmography. and with bronchoalveolar lavage (BAL) 2 4 h later. The BAL fluid was analysed for the presence of inflammatory cells and concentrations of proteins and phospholipids. Surfactant in the remaining BAC fluid was concentrated five-times and examined with a capillary surfactometer (CS), The surfactant was then washed with a large volume of saline solution which was removed following centrifug ation. Already, after a 2 h ozone exposure, the respiratory frequency increased from 297+/-6 to 386+/-11 breaths.min(-1) (p<0.0001). Pressur e amplitude per breath diminished (p<0.001), indicating a reduced tida l volume. A highly significant surfactant dysfunction was observed wit h the CS (p<0.0001), although phospholipids increased. However, protei ns also increased (p<0.0001) and they or other water-soluble inhibitor s apparently caused the surfactant dysfunction since, when they were r emoved with a washing procedure, the surfactant's normal ability to ma intain patency was restored. The acute ozone exposure affected breathi ng and caused an airway inflammation. The inflammatory proteins or oth er water-soluble inhibitors reduced the surfactant's ability to secure airway patency.