Effect of salbutamol on dry air- and acetylcholine-induced bronchoconstriction in the canine lung periphery

Abstract

We examined the effect of salbutamol on dry airflow-induced bronchoconstriction (AIB) and acetylcholine-induced bronchoconstriction (Ach-IB) in the canine lung periphery using a wedged bronchoscope technique. Collateral system resistance (Rcs) and airway wall temperature (Taw) were monitored in a peripheral lung segment before, during and after airflow challenge. Rcs before and after aerosolized acetylcholine was recorded in a contralateral lung segment. Intravenous salbutamol (2.5 micrograms.kg-1) significantly attenuated the peak fall in Taw during airflow challenge and the peak rise in Rcs following challenge. Intravenous salbutamol attenuated Ach-IB to a similar degree. Significant systemic effects were recorded following i.v. salbutamol. In contrast, aerosolized salbutamol (50 micrograms) minimally decreased the fall in Taw during airflow challenge, while virtually eliminating AIB. The same dose of aerosolized salbutamol only partially attenuated Ach-IB. Aerosolized salbutamol did not affect mean arterial pressure or heart rate. Intravenous salbutamol may in part inhibit AIB by increasing pulmonary blood flow, secondary to its systemic circulatory effects, and decrease heat and water loss during airflow challenge. In contrast, aerosolized salbutamol abolished AIB, while only minimally effecting airway cooling. These data suggest that AIB is a result of mediator release and/or smooth muscle contraction.

No influence of airway heat flux on airflow-induced bronchospasm

“…time course of bronchoconstriction after exposure to cool dry air (1,6] including a dose-response relationship [1,7]; b) the attenuation of AIB when warm humid air is substituted for cool dry air (1,4,8]; c) bronchoconstriction in response to hypertonic aerosol challenge (9,10]; d) the attenuation of AIB after pretreatment with atropine [4,11], albuterol [12,13], and aminophylline [12,14); and e) detection of mediators in bronchoalveolar lavage fluid immediately after AIB [3]. Considering these similarities, we believe that data from this model can provide considerable insight into the mechanisms involved in exercise-induced asthma.…”