RESUMO
Acute ozone (O3) exposures produce an increase in the apparent permeability of the tracheal epithelium, but the mechanism of this response is poorly understood. Comparison of previous studies suggests that qualitative differences may exist between measurements made in vivo or in vitro. To test this possibility we used both in vitro and in vivo electrophysiological techniques to investigate the effects of O3 exposure on guinea pig tracheal epithelium. Male Hartley guinea pigs were exposed to either 1 or 2 ppm O3 or to filtered air for 3 h and were studied 0, 6, or 24 h after exposure. Air-exposed animals had in vitro mean tracheal potential (VT) -32.0 +/- 1.5 mV, conductance (GTL) 2.18 +/- 0.22 mS/cm, short-circuit current (ISCL) 62.6 +/- 3.7 microA/cm, and diameter (D) 2.44 +/- 0.10 mm. In vitro properties after 1 ppm O3 exposure did not differ at any time point from control. Two parts per million O3 increased ISCL, but only at 6 h postexposure. The effect of O3 on ISCL was abolished by amiloride. There were no significant changes in VT, GTL, or D. In vivo tracheal potential under pentobarbital anesthesia was -19.7 +/- 1.7 mV. At 6 h postexposure to 2 ppm O3, but not at 0 or 24 h, in vivo VT was increased. Thus, acute exposure of guinea pigs to a high concentration of O3 caused a delayed increase in Na+ absorption by the trachea with no change in conductance. This indicates that paracellular permeability of guinea pig tracheal epithelium was not substantially increased by acute O3 and suggests that enhanced macromolecular uptake in this species probably occurs transcellularly. Furthermore, the increase of in vivo VT following O3 exposure is consistent with the in vitro response, indicating that in vivo/in vitro differences are not responsible for the discrepancies between previous electrophysiological and "permeability" studies.
