Canessa P A, Torraca A
Presidio di Pneumotisiologia, U.S.L. 28_-Bologna Nord.
Medicina (Firenze). 1990 Jul-Sep;10(3):296-8.
The occurrence of a dry, nonproductive cough during ACE inhibitors therapy has been described in several reports. However, the mechanism of this effect is still unknown. In order to clarify whether ACE inhibitor-induced cough is a symptom of an asthmatic disturbance, six patients (age 54-68) with cough related to captopril or enalapril were rechallenged with ACE inhibitors after an adequate washout period. Baseline airway function and bronchial reactivity to metacholine were measured at the end of the washout period and on the fourth day of rechallenge which was accompanied by the reappearance of cough without wheezing. Rechallenge did not cause changes in dynamic lung function; a low and not significant (p less than 0.1) increase in metacholine dose causing a 15% and a 20% reduction in baseline FEV 1 was observed. It is concluded that cough and bronchoconstriction are likely to be mediated through different nervous pathways and that ACE inhibitor-induced cough is not a variant of asthmatic cough.
多篇报告描述了在使用血管紧张素转换酶(ACE)抑制剂治疗期间出现干咳、无痰咳嗽的情况。然而,这种效应的机制仍不清楚。为了阐明ACE抑制剂引起的咳嗽是否是哮喘紊乱的一种症状,对6例(年龄54 - 68岁)与卡托普利或依那普利相关咳嗽的患者,在经过适当的洗脱期后再次给予ACE抑制剂。在洗脱期末以及再次激发的第4天测量基础气道功能和对乙酰甲胆碱的支气管反应性,再次激发时伴有咳嗽再现但无喘息。再次激发未引起动态肺功能改变;观察到乙酰甲胆碱剂量有轻微且无统计学意义(p<0.1)的增加,导致基础第一秒用力呼气容积(FEV₁)降低15%和20%。得出的结论是,咳嗽和支气管收缩可能通过不同的神经途径介导,且ACE抑制剂引起的咳嗽不是哮喘性咳嗽的一种变异型。