Bronchospasm-evoked

Aspirin, cyclooxygenase, and the provocation of asthma A few people with asthma suffer from a unique syndrome in which the ingestion of 40 to 300 mg of aspirin produces rhinorrhea and acute bronchoconstriction. All cyclooxygenase inhibitors will precipitate bronchospasm in patients with aspirin-evoked asthma. 

The parasympathetic division is the dominant portion of the pulmonary autonomic nervous system in all mammals. Airway smooth muscle is richly supplied with muscarinic receptors and stimulation of M3 receptors results in smooth muscle contraction and bronchoconstriction. Cholinergic stimulation is the primary mechanism of bronchospasm in horses with recurrent airway obstruction (Robinson et al 1996). Parasympathetic innervation can be demonstrated throughout the tracheobronchial tree of the horse but smooth muscle contraction evoked by stimulation of cholinergic nerves is more pronounced in the trachea than in the smaller bronchi. It is expected that parasympathetic blockade with a muscarinic antagonist will have the greatest effect in large, central airways. 

EXTRAVASCULAR SMOOTH MUSCLE Histamine stimulates or, more rarely, relaxes various extravascular smooth muscles. Contraction is due to activation of H j receptors (linked to and Ca + mobilization) relaxation (for the most part) is due to activation of Hj receptors. Minute doses of histamine will evoke intense bronchoconstriction in patients with bronchial asthma and certain other pulmonary diseases. Although the spasmogenic influence of Hj receptors is dominant in bronchial muscle, receptors with dilator function also are present. Thus, histamine-induced bronchospasm is potentiated slightly by blockade. 

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