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This effectively prevents bronchoconstriction in response to parasympathetic stimulation. They may be used in combination with other bronchodilators. Antimuscarinics are of particular use in chronic bronchitis where the airways seem resistant to β because they also reduce mucus secretion. They are most frequently used as aerosol inhalers and in nebulizers.
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It is not known exactly how antiepileptic drugs work, but two mechanisms seem to be important for drugs in current use, while newer drugs may work by other means yet to be elucidated. Many well-established antiepileptic drugs (for example phenobarbital and benzodiaze pines) are known to facilitate the opening of GABA chloride ion channels at synapses. However, this is not the complete explanation as, for example phenobarbital is far more effective as an anticonvulsant than other barbiturates with the same enhancing effects on GABA. Newer drugs have been shown to interfere with GABA in other ways: by inhibiting GABA-transaminase, the enzyme responsible for inactivating GABA (vigabatrin and valproate) or by directly stimulating GABA receptors. Sodium ion channels in the neuronal membrane open during the depolarization phase of an action potential.
Current examples are montelukast and zafirlukast, both of which are given orally, either alone or in combination with corticosteroids. They are not recommended for use in chronic bronchitis. Side effects of leukotriene receptor antagonists are gastrointestinal disturbances and headache. Corticosteroids are anti-inflammatory drugs that can be used in asthma to reduce airway hyper-responsiveness and to decrease bronchial oedema and mucus secretion. They are effective in the late phase reaction and reduce the intensity of allergic reactions.
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Authored by Natalie Kurtz, MD, MS, FAAP