Boulet L P, Milot J, Lampron N, Lacourcière Y
Pulmonary Research Unit, Laval Hospital, Sainte-Foy, Quebec, Canada.
JAMA. 1989 Jan 20;261(3):413-6.
Angiotensin-converting enzyme inhibitors sometimes cause cough; the mechanism is unknown. We therefore studied the effects of ambulatory treatment with captopril on pulmonary function and on nonspecific bronchial responsiveness to methacholine in 15 hypertensive subjects. Lung volumes, expiratory flows and nonspecific bronchial responsiveness to methacholine using doses up to 64 g/L were measured before and four and eight weeks after captopril treatment was started. Throughout the study the subjects recorded respiratory symptoms and peak expiratory flow rates. In four subjects a persistent cough developed related to the use of captopril, but this was not associated with the development of airflow obstruction or bronchial hyperresponsiveness. The mean provocative concentration of methacholine that resulted in a 20% fall in the forced expiratory volume in 1 s was 43.6 +/- 1.8 g/L after eight weeks of captopril treatment compared with 61.6 +/- 1.2 g/L at the baseline evaluation. We concluded that there was no significant change in lung function during treatment with captopril. The development of a cough related to this medication is not associated with the development of airflow obstruction or airway hyperresponsiveness.
血管紧张素转换酶抑制剂有时会引起咳嗽，其机制尚不清楚。因此，我们研究了卡托普利门诊治疗对15名高血压患者肺功能以及对乙酰甲胆碱非特异性支气管反应性的影响。在开始卡托普利治疗前、治疗4周和8周后，测量肺容积、呼气流量以及使用剂量高达64μg/L的乙酰甲胆碱时的非特异性支气管反应性。在整个研究过程中，受试者记录呼吸道症状和呼气峰值流速。4名受试者出现了与使用卡托普利相关的持续性咳嗽，但这与气流阻塞或支气管高反应性的发生无关。卡托普利治疗8周后，导致第1秒用力呼气量下降20%的乙酰甲胆碱平均激发浓度为43.6±1.8μg/L，而基线评估时为61.6±1.2μg/L。我们得出结论，卡托普利治疗期间肺功能无显著变化。与该药物相关的咳嗽的发生与气流阻塞或气道高反应性的发生无关。
