Popio K A, Jackson D H, Utell M J, Swinburne A J, Hyde R W
Chest. 1983 Feb;83(2):175-9. doi: 10.1378/chest.83.2.175.
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.
禁用普萘洛尔诱发的支气管痉挛有时会妨碍在慢性阻塞性肺疾病（COPD）患者中使用该药。通过吸入拟副交感神经药物卡巴胆碱和异丙肾上腺素进行支气管激发试验，已开发出一种方法来识别发生这种不良反应风险较高的患者。在进行基线肺功能测试后，12例不同程度COPD患者和13例对照患者在心脏导管插入术期间静脉注射普萘洛尔进行最大程度的β受体阻滞，随后重复进行肺功能测试。7例COPD患者和10例对照受试者在口服普萘洛尔至少三周后再次接受研究。结果表明，吸入异丙肾上腺素后的支气管扩张反应不能可靠地识别出使用普萘洛尔后发生支气管收缩的患者，但吸入卡巴胆碱后的支气管收缩表明发生普萘洛尔诱发支气管收缩的高风险。
