Abstract

The present study is a continuation of our previous experiments on repeated 10-min exposures of anesthetized, mechanically ventilated guinea pigs to clean cold dry air (Hälinen et al., 2000a), and to cold air plus gaseous air pollutants (Hälinen et al., 2000b). This time we made continuous 60-min exposures to clean cold dry air, cold air + SO2 at 1 ppm, cold air + NO2 at 1 ppm, and warm humid air + NO2 at 1 ppm, and focused on responses at 10-60 min. Clean cold dry air and cold air + pollutants (n = 8-9 in each group) produced similar cooling in the guinea pig lower respiratory tract. The decreases in intratracheal temperature (Ttr) reached a plateau at 20 min with mean maximal decreases of 9.7-11.3°C from the pre-exposure control values of 36.0-37.3°C. In contrast, there were progressive decreases in esophageal temperature (Toe) during the exposures, indicating constant conductive and evaporative heat losses from the tracheobronchial tissues. The mean maximal decreases in Toe were 1.2-1.4°C from the preexposure control values of 37.8-38.0°C. Clean cold dry air induced 4.5-10.8% mean decreases in peak expiratory flow (PEF) at 10-60 min of exposure, which were statistically nonsignificant due to a relatively large variation between animals. Cold air + SO2 at 1 ppm induced a mean decrease of 11.4% in PEF at 10 min (p < .05), which was spontaneously abolished during the next 10 min of exposure. Cold air + NO2 at 1 ppm caused no decrease, but in fact small, nonsignificant increases in PEF at 30-60 min of exposure. Cold air + NO2 at 1 ppm, and to some extent also cold air + SO2 at 1 ppm, attenuated significantly the mechanical ventilation induced gradual decrease in tidal volume (VT), when compared to clean cold dry air exposure. Cold air + NO2 at 1 ppm, but not warm humid air + NO2 at 1 ppm, increased significantly the proportion of macrophages in the differential count of bronchoalveolar lavage fluid (BALF) white cells when compared to both clean warm humid air and cold dry air. None of the exposure conditions caused morphological or inflammatory changes in the respiratory tissues. In conclusion, continuous 60-min exposures to clean cold dry air, cold air + SO2, and cold air + NO2 produced weaker functional effects on the lower respiratory tract of guinea pigs than our previous consecutive 10-min exposures to these air conditions. After the first 10 min, there was a strong attenuation of the bronchoconstrictor responses, especially to cold air + NO2 at 1 ppm. The small airway effects of prolonged mechanical ventilation were significantly modified by NO2 at 1 ppm in both cold dry and warm humid breathing air. Finally, cold air + NO2 at 1 ppm increased the proportion of macrophages in BALF white cells.

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