P7 Neuronal Dysfunction In Asthma; Insights From The Study Of The Cough Reflex

Introduction Cough in asthma is common, troublesome, predicts severity and poor prognosis, yet remarkably little is understood about the underlying neuronal mechanism. Currently available asthma medications are not designed to directly treat cough, the archetypal airway neuronal reflex. Previous studies have commonly used the dose of capsaicin that evokes two coughs (C2) or five coughs (C5) as the standard measure to assess the sensitivity of the cough reflex. These measures poorly discriminate between health and disease, and correlate only weakly with objective cough rates.2 A novel challenge methodology that uses the maximum number of evoked coughs (Emax) as an end point better discriminates between health and disease and correlates strongly with subjective cough measures.2 Objective To assess the differences in the maximum cough responses evoked by capsaicin (Emax) between asthmatics and healthy volunteers. Method A capsaicin inhalational challenge (doubling doses 0.49 to 1000[micro]M) was performed. Four inhalations 30 seconds apart were performed at each concentration and the total coughs evoked at each dose were recorded and verified using a cough monitor. The highest total number of coughs evoked at any dose of capsaicin is denoted Emax.