Ozone-induced decrease of mouse tracheal potential is not secondary to cellular inflammation

Acute exposure of C57BL/6J (B6) mice to ozone (O3) causes decreased in vivo tracheal electrical potential difference (PD). To investigate the role of inflammation in this response we measured O3 effects in B6 mice pretreated with indomethacin (5 mg/kg), colchicine (3 mg/kg), or cyclophosphamide (30 mg/kg x 7 days). Mice were exposed to 2 ppm O3 or air for 3 hr and allowed to recover for 0, 3, 6, 9, or 12 hr. Tracheal PD was measured under pentobarbital anesthesia using a capped agar bridge inserted into the upper trachea through a neck incision. After measurement of PD, bronchoalveolar lavage (BAL) was performed and total cells, polymorphonuclear leukocytes (PMNs), and protein were determined. As previously reported, O3 exposure decreased PD and increased BAL total cells, PMNs, and protein. O3-induced changes in PD and PMNs were maximal 6-9 hr after exposure. Indomethacin prevented the O3-induced change in PD but had no effect on BAL total cells or PMNs. Colchicine attenuated O3-induced increases in PMNs and cyclophosphamide decreased O3 effects on both BAL total cells and PMNs but neither drug affected the PD response. None of the drugs significantly altered O3-induced increases in BAL protein. The indomethacin sensitivity of O3-induced changes in PD may reflect a role of cyclooxygenase products in that response. However, drugs known to inhibit PMN function did not affect O3-induced changes in PD. We suggest that cellular inflammation is not required for the tracheal electrophysiological response to acute O3 exposure.