To overcome intractable chronic cough: disclosure of mechanism of cough response to bronchoconstiction to conrol of the cough

基础研究：β 2激动剂可消除甲基苯丙胺引起的支气管收缩和咳嗽。辣椒素脱敏对支气管收缩和咳嗽次数无影响。莫古斯汀抑制咳嗽次数，但对支气管收缩无抑制作用。结论支气管收缩通过RARs引起咳嗽，而不是通过c -纤维引起咳嗽。此外，前列腺素E2可增强甲基苯丙胺诱导的咳嗽反应，保护支气管收缩。临床研究：咳嗽变异性哮喘患者对甲基苯丙胺所致支气管收缩的咳嗽反应增高。治疗后咳嗽反应恢复到正常范围。因此，我们确定支气管收缩引起的咳嗽反应增强是咳嗽变异性哮喘的基本生理特征。咳嗽反应性Mch对区分咳嗽变异性哮喘和慢性非生产性咳嗽的敏感性和特异性分别为81.0%和89.7%。

Basic study: Beta2-agonists abolished both the methacholine-induced bronchoconstriction and cough. Capsaicin desensitization had no effect on the bronchoconstriction or the number of coughs. Moguisteine inhibited the number of coughs but not the bronchoconstriction. It is concluded that bronchoconstriction causes cough via RARs, but not C-fibers. Furthermore, prostaglandin E2 takes a role to enhance the methacholine-induced cough response as protection of bronchoconstriction.Clinical study: Cough response to bronchoconstriction induced by Meth was heightened in cough variant asthma patients. The increased cough response recovered to normal range after treatment. Thus, we identified heightened cough response to bronchoconstriction as a fundamental physiologic feature of cough variant asthma. Sensitivity and specificity of cough responsiveness to Mch for discrimination of cough variant asthma from chronic non-productive cough were 81.0% and 89.7%, respectively.