Freed A N, Chou C L, Fuller S D, Croxton T L
Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA.
Respir Physiol. 1996 Aug;105(1-2):95-102. doi: 10.1016/0034-5687(96)00040-0.
We examined the effects of ozone (O3) on central and peripheral airway reactivity and tracheal transepithelial potential difference (PD) in New Zealand white rabbits. Rabbits were exposed for 7 h to either room temperature-humidified filtered air (n = 7) or 0.2 ppm O3 in humidified room air (n = 5). Tracheal PD was recorded 3 h after exposure. Whole lung resistance (RL) and reactivity were partitioned into their central (RC) and peripheral (RP) components using a retrograde catheter and forced oscillation. Changes in RL, RC, and RP in response to NaCl (0.9%) and ACh (100 mM) aerosol challenges were measured before and after vagotomy. Exposure to O3 decreased tracheal PD from -29 +/- 0.6 mV in air-exposed rabbits to -15 +/- 2 mV in O3-exposed rabbits (p < or = 0.0001). Exposure to O3 did not alter RL, RC, or RP. However, the ACh-induced increase in RL in O3-exposed rabbits (140%) was twice that recorded in the air-exposed group (p < or = 0.01). While changes in RP dominated the whole lung response to ACh in air-exposed rabbits, changes in RC were most prominent in the O3-exposed group. Bilateral vagotomy did not alter airway reactivity in control rabbits but did enhance peripheral lung reactivity in O3-exposed rabbits. We conclude that exposure to 0.2 ppm O3 for 7 h affects tracheal epithelial function in rabbits and increases central airway reactivity via vagal mechanisms without altering baseline RL, RC, or RP.
