OZONE-INDUCED VAGAL REFLEX MODULATES AIRWAYS REACTIVITY IN RABBITS

We examined the effects of ozone (O-3) on central and peripheral airwa y reactivity and tracheal transepithelial potential difference (PD) in New Zealand white rabbits. Rabbits were exposed for 7 h to either roo m temperature-humidified filtered air (n = 7) or 0.2 ppm O-3 in humidi fied room air (n = 5). Tracheal PD was recorded 3 h after exposure. Wh ole lung resistance (R(L)) and reactivity were partitioned into their central (R(C)) and peripheral (R(P)) components using a retrograde cat heter and forced oscillation. Changes in R(L), R(C), and R(P) in respo nse to NaCl (0.9%) and ACh (100 mM) aerosol challenges were measured b efore and after vagotomy. Exposure to O-3 decreased tracheal PD from - 29 +/- 0.6 mV in air-exposed rabbits to -15 +/- 2 mV in O-3-exposed ra bbits (p less than or equal to 0.0001). Exposure to O-3 did not alter R(L), R(C), or R(P). However, the ACh-induced increase in R(L) in O-3- exposed rabbits (140%) was twice that recorded in the air-exposed grou p (p less than or equal to 0.01). While changes in R(P) dominated the whole lung response to ACh in air-exposed rabbits, changes in R(C) wer e most prominent in the O-3-exposed group. Bilateral vagotomy did not alter airway reactivity in control rabbits but did enhance peripheral lung reactivity in O-3-exposed rabbits. We conclude that exposure to 0 .2 ppm O-3 for 7 h affects tracheal epithelial function in rabbits and increases central airway reactivity via vagal mechanisms without alte ring baseline R(L), R(C), or R(P).