Characterization of respiratory exposure to and effects of cold-air hyperventilation in guinea pigs.

The purpose of this study was to characterize the respiratory effects of single and repeated controlled exposures to clean warm humid and cold dry air in a new model of anesthetized, mechanically ventilated guinea pigs, and to compare findings with known effects in humans. Intratracheal air (T(tr)) and retrotracheal tissue (T(oe)) temperatures and peak expiratory airflow (PEF), tidal volume (V(T)), heart rate, and blood pressure of hyperventilating animals were measured continuously. Four consecutive 10-min exposures to warm humid air (n = 7) produced slight airway warming and minimal lung function changes during the exposure. In a single 10-min exposure to cold dry air (n = 39), T(tr) decreased from (means +/- SEM) 36.1 +/- 0.3 degrees C to 26.3 +/- 0.3 degrees C (Delta = -9.8 +/- 0.4 degrees C) and T(oe) from 36.4 +/- 0.2 degrees C to 35.5 +/- 0.2 degrees C (Delta = -0.9 +/- 0.1 degrees C). PEF and V(T) decreased in response to airway cooling with maximal decrements within the first 2-4 min from the beginning of the exposure period. The maximal decrease in PEF was from 21.7 +/- 0.3 ml s(-1) to 15.9 +/- 0.5 ml s(-1) (Delta = -26.7%) and that in V(T) from 5.2 +/- 0.1 ml to 4.2 +/- 0.1 ml (Delta = -19.2%) (p <.05 for both changes). The decreases in lung functions attenuated significantly during the course of the 10-min exposure to cold dry air, indicating adaptation. Consequently, the decrements in PEF and V(T) at 5, 7.5, and 10 min were significantly smaller than those at 3 min. In four consecutive 10-min exposures to cold dry air (n = 15), there were no statistically significant differences in T(tr) or T(oe) decreases between the exposure periods. The largest decreases in the lung function parameters were during the first exposure period, whereas there were significantly smaller responses during the second and third exposure periods (p <.05). Thus, a highly reproducible airway cooling and an immediate bronchoconstriction were produced in response to cold dry air hyperventilation in guinea pigs. During the course of cold-air exposure and in repeated exposures, there was a significant attenuation of the bronchial response, which resembled the refractoriness of the asthmatic airways to repeated hyperventilation of cold or warm dry air. The present guinea pig model seems to be well suited for production of complementary animal data on the pathophysiological effects of cold dry air on the tracheobronchial airways.