Bronchoconstriction/bronchial hyperreactivity

Bronchodilators are helpful in individuals with cough and bronchoconstriction due to bronchial hyperreactivity. They help by improving the effectiveness of cough in clearing secretions. 

Whatever the mechanisms responsible for bronchial hyperreactivity, bronchoconstriction itself seems to result not simply from the direct effect of the released mediators but also from their activation of neural or humoral pathways. Evidence for the importance of neural pathways stems largely from studies of laboratory animals. Thus, the bronchospasm provoked in dogs by histamine can be greatly reduced by pretreatment with an inhaled topical anesthetic agent, by transection of the vagus nerves, and by pretreatment with atropine. Studies of asthmatic humans, however, have shown that treatment with atropine causes only a reduction in—not abolition of—the... 

The role of peptidergic neurons is not so clear. Capsaicin, the hot chile pepper chemical that evokes release of peptide transmitters from several types of sensory nerves, has been shown to reproduce some of the signs of bronchial hyperreactivity in animal and human experiments. These findings led to the proposal that sensitization of afferent nerve endings played a major role in chronic airway hyperreactivity. However, peptide transmitter antagonists have not been able to prevent bronchoconstriction in several models. Clearly, much remains to be learned about airway pharmacology. 

The importance of PAF in airway hypersensitivity has been confirmed by the protective effect exerted by BN 52021 and related ginkgolides [192] in (i) PAF-induced bronchoconstriction and airway hyperreactivity in both humans and animals (ii) various models of immune anaphylaxis and airway hyperreactivity in animals and, as we shall discuss later (iii) antigen-induced bronchial provocation tests in asthmatic patients. 

In addition to tracheobronchial secretions, bronchial smooth muscle is stimulated by the muscarinic agonists. Asthmatic patients respond with intense bronchoconstriction, secretions, and a reduction in vital capacity. These actions form the basis of the methacholine challenge test used to diagnose airway hyperreactivity. 

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