Airflow-induced Bronchospasm: Imbalance between Airway Cooling and Airway Drying?

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Abstract
We used an animal model of airflow-induced bronchospasm (AIB) to examine the role of airway cooling in responses to dry air challenge. A bronchoscope was wedged in situ into perfused lower lobes of anesthetized dogs. Through the bronchoscope, dry air was delivered, resistance to collateral flow (Rcs) was measured, and airway wall temperature (Taw) was monitored. A dry-air challenge through the bronchoscope produced a fall in Taw and a rise in Rcs, presumably related to evaporative heat loss (EHL) and/or an increase in osmolarity. By changing the temperature of blood perfusing the lobe it was possible to lower Taw without affecting either EHL or osmolarity. Four series of experiments were performed. In the first series, Taw was lowered in 2 ways: by increasing dry air flow and by cooling the pulmonary perfusate. After a 2-min challenge with dry air, Rcs rose. After lowering Taw with cooled blood for 2 min, Rcs did not rise. In the second series of studies, Taw was lowerd for 15-min periods by reducing the temperature of blood. Neither cooling per se nor rewarming after the 15 min of cooling initiated increases in lung tone. In the third series of experiments, a 2-min dry air challenge was performed while the lobe was perfused with cool blood. Despite greater reductions in Taw during the dry-air challenge, responses after the challenge were virtually abolished. In a final series of experiments in which pulmonary perfusion was stopped during challenge, airway cooling was enhanced, and responses were again significantly attenuated. Thus, cooling actually depressed increases in Rcs produced by dry-air challenge. We hypothesize that AIB is the result of an imbalance between 2 regularly but opposing pathways, one controlling airway cooling (inhibitory) and the other controlling drying (excitatory).