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Chest, Vol 83, 175-179, Copyright © 1983 by American College of Chest Physicians
ARTICLES |
KA Popio, DH Jackson Jr, MJ Utell, AJ Swinburne and RW Hyde
Disabling propranolol-induced bronchospasm occasionally prevents use of this drug in patients with chronic obstructive pulmonary disease (COPD). A means was developed to identify patients who have high risk for this adverse effect using bronchial challenge by inhaling the parasympathomimetic drug, carbachol, and isoproterenol. After baseline pulmonary function tests, 12 patients with varying degrees of COPD and 13 control patients underwent maximal beta-blockade using intravenously administered propranolol during cardiac catheterization followed by repeat pulmonary function testing. Seven of the patients with COPD and ten of the control subjects were restudied while taking propranolol orally for at least three weeks. The results indicated that the bronchodilator response to inhaled isoproterenol does not reliably identify patients who develop bronchoconstriction with propranolol, but bronchoconstriction after inhaling carbachol is indicative of the high risk of developing bronchoconstriction from propranolol.
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