Boulet L P, Latimer K M, Roberts R S, Juniper E F, Cockcroft D W, Thomson N C, Daniel E E, Hargreave F E
Am Rev Respir Dis. 1984 Sep;130(3):368-72. doi: 10.1164/arrd.1984.130.3.368.
We examined the role of cholinergic mechanisms in causing the increase in histamine bronchial responsiveness that follows allergen exposure. Five stable adult atopic asthmatics received inhalation tests with histamine on 2 days after both placebo and a dose of atropine sulphate (18 mg nebulized during tidal breathing), which reduced saliva output. On a third day, an allergen inhalation test was carried out to stimulate a dual asthmatic response. When the FEV1 had returned to within 10% of baseline, the histamine test was repeated after placebo and atropine. Before allergen inhalation, atropine marginally increased the FEV1 (p = 0.12) and reduced bronchial responsiveness to histamine (p = 0.003). When allergen challenge had induced an increase in histamine responsiveness (p = 0.001), atropine again marginally increased FEV1 (p = 0.063) and reduced the responsiveness (p = 0.004) but did not return the responsiveness to the preallergen level (p = 0.023). There was no evidence that the magnitude of the atropine blockade of histamine responsiveness was different before and after allergen (p = 0.92). We conclude that cholinergic mechanisms are not likely to explain the increase in bronchial responsiveness that follows allergen-induced inflammation.
我们研究了胆碱能机制在引发变应原暴露后组胺支气管反应性增加中所起的作用。五名病情稳定的成年特应性哮喘患者在接受安慰剂和一剂硫酸阿托品（潮气呼吸时雾化吸入18毫克）治疗后的两天，分别进行了组胺吸入试验，硫酸阿托品可减少唾液分泌。在第三天，进行变应原吸入试验以激发双重哮喘反应。当第一秒用力呼气量（FEV1）恢复到基线的10%以内时，在给予安慰剂和阿托品后重复进行组胺试验。在吸入变应原之前，阿托品使FEV1略有增加（p = 0.12），并降低了对组胺的支气管反应性（p = 0.003）。当变应原激发导致组胺反应性增加时（p = 0.001），阿托品再次使FEV1略有增加（p = 0.063）并降低了反应性（p = 0.004），但未使反应性恢复到变应原激发前的水平（p = 0.023）。没有证据表明变应原前后阿托品对组胺反应性的阻断程度有所不同（p = 0.92）。我们得出结论，胆碱能机制不太可能解释变应原诱导的炎症后支气管反应性的增加。
