Okayama M, Yafuso N, Nogami H, Lin Y N, Horio S, Hida W, Inoue H, Takishima T
J Allergy Clin Immunol. 1987 Sep;80(3 Pt 1):291-9. doi: 10.1016/0091-6749(87)90034-0.
To establish a safe procedure for examining propranolol-induced bronchoconstriction, we have developed a new method for performing inhalation challenge with propranolol. Monitoring respiratory resistance during tidal breathing with continuous inhalation of propranolol in 1.5-fold increasing concentrations from 0.78 to 30 mg/ml for 1 minute at each concentration, we tested 43 subjects with stable asthma and 10 normal subjects. We also compared bronchial responsiveness with responsiveness to inhaled methacholine on separate days. In addition, to determine the role of vagal nerve activity in propranolol-induced bronchoconstriction, we studied the effect of atropine. Inhaled propranolol caused dose-related bronchoconstriction in all subjects with asthma but not in normal subjects. None of the subjects suffered severe asthmatic attack during the test, which was performed in 15 minutes or less. The minimum cumulative dose of methacholine and of propranolol, at the point where respiratory conductance began to decrease, was not significantly correlated. Increased respiratory resistance was reversed by atropine in 70% of the subjects with asthma with marked individual differences. These data suggest that, although in most subjects with asthma, vagal nerve activity contributes in varying degree to bronchoconstriction, other constricting factors may contribute in the remaining subjects. It is also suggested that the mechanism of bronchial response to propranolol differs from that of the nonspecific airway reactivity estimated by methacholine challenge.
为建立一种检测普萘洛尔诱发支气管收缩的安全方法，我们开发了一种用普萘洛尔进行吸入激发试验的新方法。在潮式呼吸过程中监测呼吸阻力，以0.78至30mg/ml的浓度连续吸入普萘洛尔，每次浓度递增1.5倍，持续1分钟，我们对43名稳定期哮喘患者和10名正常受试者进行了测试。我们还在不同日期比较了支气管反应性与对吸入乙酰甲胆碱的反应性。此外，为确定迷走神经活动在普萘洛尔诱发支气管收缩中的作用，我们研究了阿托品的效果。吸入普萘洛尔在所有哮喘患者中均引起剂量相关的支气管收缩，但在正常受试者中未引起。在15分钟或更短时间内进行的测试中，没有受试者发生严重哮喘发作。在呼吸传导开始下降时，乙酰甲胆碱和普萘洛尔的最小累积剂量无显著相关性。70%的哮喘患者中，阿托品可逆转呼吸阻力增加，且个体差异明显。这些数据表明，虽然在大多数哮喘患者中，迷走神经活动在不同程度上导致支气管收缩，但在其余患者中可能有其他收缩因素起作用。还表明，支气管对普萘洛尔的反应机制与乙酰甲胆碱激发试验所估计的非特异性气道反应性机制不同。
