Inhaled muscarinic antagonists have so far earned a limited place in the treatment of asthma. The effects of short-acting agents (eg, ipratropium bromide) on baseline airway resistance is nearly as great as, but no greater than, those of the sympathomimetic drugs, so they are used largely as alternative therapies for patients intolerant of β2-adrenoceptor agonists. The airway effects of anti-muscarinic and sympathomimetic drugs given in full doses have been shown to be additive only in patients with severe airflow obstruction who present for emergency care.
The long-acting antimuscarinic agent tiotropium has not yet earned a place in the treatment for asthma, although it has been shown to be as effective as a long-acting β2-agonist when used in addition to an inhaled corticosteroid treatment for that condition. As a treatment for COPD, tiotropium both improves functional capac-ity, presumably through its action as a bronchodilator, and reduces the frequency of exacerbations, through mechanisms not yet defined.
Although it was predicted that muscarinic antagonists would dry airway secretions and interfere with mucociliary clearance, direct measurements of fluid volume secretion from single airway submucosal glands in animals show that atropine decreases base-line secretory rates only slightly. The drugs do, however, inhibit the increase in mucus secretion caused by vagal stimulation. No cases of inspissation of mucus have been reported following administration of these drugs.