Abstract
For the purposes of this article I will define asthma as an inflammatory airway disease characterized by variable obstruction of the tracheobronchial tree in which the airways narrow too much and too easily in response to a variety of triggers that have little or no effect in the normal lung. This definition has three components: airway inflammation, excessive airway narrowing in response to agents that normally have a trivial effect, and variability of airway obstruction. Of these three components, airway inflammation has received a great deal of attention, particularly in the last 2 decades. Airway narrowing that is excessive and occurs too easily has been studied extensively by dose-response curves to a variety of triggers of airway narrowing. We now know that the reason that airways narrow too much is either because the smooth muscle lining the tracheobronchial tree develops an increased force or the load it is acting on is diminished. However, we know very little about the mechanisms underlying the variability of airway obstruction, even though we knew of its existence long before we knew much about airway inflammation and bronchial dose-response curves. Indeed, although it has proven impossible to define asthma in a way acceptable to all, it is agreed that variability of airway obstruction must be included in any definition of asthma.
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