Bronchial hyperresponsiveness is not bronchial hyperresponsiveness is not bronchial asthma

Bronchial hyperresponsiveness is regarded as a major characteristic of bronchial asthma [1,2]. Patients with bronchial asthma have an increased airway responsiveness to various bronchoconstrictor stimuli including chemical agents, such as histamine, methacholine and leukotrienes, and physical stimuli, such as cold air; hyperventilation and exercise (Table 1). A good correlation has been observed between the responsiveness to some ofthese chemical and physical stimuli [3]. The term 'non-specific' has been coined to differentiate this type of airway hyperresponsiveness, which affects almost all asthmatic subjects, from the response to specific stimuli such as allergens or occupational agents. The aim of the present paper is to emphasize that the various stimuli usfed to assess non-specific bronchial responsiveness act through different bronchoconstrictor mechanisms. Furthermore, we postulate that these differences are important determinants when studying the relationship between bronchial hyperresponsiveness and bronchial asthma or the effect of anti-asthmatic drugs on bronchial responsiveness. In asthmatics, acute bronchoconstriction can be provoked by several stimuli, including allergens, exercise, cold air, fog, air pollutants, cigarette smoke, and the intake of drugs such as aspirin. The mechanisms involved in the acute bronchial response to these triggers are partially understood and summarized in Table 2. The bronchoconstrictor response to different stimuli is mediated (i) via interaction with receptors situated on the bronchial smooth muscle cells, (ii) via interaction with receptors on inflammatory cells such as mast cells and macrophages, leading to the liberation of mediators that act on the smooth muscle cells or nerve receptors, or (iii) by stimulation of the sensory nerve receptors leading to local axon reflexes or vagally mediated central nervous reflexes. In-vitro investigations in man have shown that there are interindividual differences in the responsiveness of isolated bronchial smooth

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