Effect of rapid shallow breathing on the distribution of 18O-labeled ozone reaction product in the respiratory tract of the rat.

We examined the effect of breathing pattern on ozone reaction product content within the respiratory tract. Thirty-four anesthetized, male Wistar rats were exposed to oxygen-18 ((18)O)-labeled ozone at 1.0 ppm for 2 h using a dual-chamber, negative-pressure ventilation system. Frequency was set at 80 (n = 9), 120 (n = 7), 160 (n = 8), or 200 (n = 10) breaths per minute (bpm), while tidal volume (V(t)) was set to provide a constant minute ventilation of 72.8 ml/min/100 g body weight. Airways sampled were from the midlevel trachea and the mainstem bronchi and parenchyma of the cranial and caudal right lobes. (18)O content in each airway sample was quantified and normalized to surface area. Across frequencies, there was significantly greater (p <.05) (18)O content in the trachea and bronchi (conducting airway epithelium) compared to the parenchyma sampling sites. Tracheal (18)O content decreased between 80 and 160 bpm, but then underwent an increase at 200 bpm. In comparison, (18)O content gradually increased between 80 and 200 bpm at the right cranial and caudal bronchi sites. Right cranial parenchymal (18)O content decreased at 200 bpm compared to 80, 120, and 160 bpm. Right caudal parenchymal (18)O content was relatively constant over all breathing frequencies. We concluded that the development of rapid shallow breathing from 80 to 160 bpm results in a reduced deposition of O(3) in the trachea, while only mildly affecting to ozone deposition in parenchyma supplied by short and long airway paths.