Oosterhoff Y, de Jong J W, Jansen M A, Koëter G H, Postma D S
Department of Pulmonology, University Hospital, Groningen, The Netherlands.
Am Rev Respir Dis. 1993 Mar;147(3):553-8. doi: 10.1164/ajrccm/147.3.553.
In contrast to methacholine, a stimulus that induces airway constriction mainly by "direct" stimulation of airway smooth muscle cells, AMP airway responsiveness reflects "indirectly" induced airway narrowing via inflammatory or neural reflex mechanisms. In order to determine inflammatory contribution to airway narrowing in COPD, we performed AMP and methacholine inhalation provocation tests in nonatopic subjects with COPD and compared the results with those obtained from atopic nonsmoking asthmatics and from healthy smoking volunteers. AMP caused airway narrowing in all but two subjects with COPD and in only three of the 12 healthy smoking subjects. Patients with COPD were significantly more responsive to AMP and methacholine than were healthy smoking volunteers. Geometric mean PC20 AMP was significantly lower in the smokers with COPD (7.2 mg/ml) than in the nonsmokers with COPD (58.5 mg/ml), whereas PC20 methacholine values and baseline FEV1 were comparable. In the nonatopic nonsmoking subjects with COPD, PC20 AMP was significantly higher than in the atopic nonsmoking asthmatics (3.8 mg/ml), whereas they responded similar to methacholine provocation. These results indicate that most subjects with COPD respond to AMP provocation and that smoking determines the degree of airway responsiveness to AMP in COPD. We suggest that increased susceptibility to mediator release by mast cells or neural reflex mechanisms are involved in AMP-induced airway constriction in asthma and in COPD.
与主要通过“直接”刺激气道平滑肌细胞诱导气道收缩的乙酰甲胆碱不同，AMP气道反应性反映了经由炎症或神经反射机制“间接”诱导的气道狭窄。为了确定炎症对慢性阻塞性肺疾病（COPD）气道狭窄的影响，我们对非特应性COPD患者进行了AMP和乙酰甲胆碱吸入激发试验，并将结果与特应性非吸烟哮喘患者及健康吸烟志愿者的结果进行比较。除两名COPD患者外，其余所有患者吸入AMP后均出现气道狭窄，而12名健康吸烟受试者中只有3人出现这种情况。COPD患者对AMP和乙酰甲胆碱的反应明显高于健康吸烟志愿者。COPD吸烟者的AMP几何平均PC20（7.2 mg/ml）显著低于COPD非吸烟者（58.5 mg/ml），而乙酰甲胆碱的PC20值和基线第一秒用力呼气容积（FEV1）相当。在非特应性非吸烟COPD患者中，AMP的PC20显著高于特应性非吸烟哮喘患者（3.8 mg/ml），而他们对乙酰甲胆碱激发试验的反应相似。这些结果表明，大多数COPD患者对AMP激发试验有反应，且吸烟决定了COPD患者对AMP的气道反应程度大小。我们认为，肥大细胞或神经反射机制导致介质释放的易感性增加与哮喘和COPD中AMP诱导的气道收缩有关。
