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M_2受体功能障碍将导致间接的迷走神经功能增强。尽管有少数观察认为慢性阻塞性肺病(COPD)时可能发生M_2受体功能障碍,但肺脏M_2受体的功能一直没有得到研究。本文研究稳定的COPD患者M_2受体的功能。 对象和方法 医院随访中的22例稳定的COPD患者入选本研究。进入研究前至少6周未使用抗生素或口服皮质激素。两个对照组为肺功能正常的11例吸烟者和13例不吸烟者。气道阻力测定采用脉冲示波测量法。鼻腔干燥冷空气激发用于诱发支气管收缩。实验对象随机接受安慰剂(0.9％盐水)、非选择性M受体阻滞剂溴化异丙托品(500μg)、选择性M_2受体激动剂匹鲁卡品(5mg/ml)的预处理。然后以干燥冷空气激发导致支气管收缩。分别测定基础的、预处理后的和冷空气激发后的气道阻力并做记录。
M 2 receptor dysfunction will lead to indirect vagal enhancements. Although few observations suggest that M 2 receptor dysfunction may occur in chronic obstructive pulmonary disease (COPD), the function of the lung M 2 receptor has not been studied. This article investigates the function of M 2 receptors in patients with stable COPD. Subjects and Methods Twenty-two patients with stable COPD during hospital follow-up were enrolled in this study. No antibiotics or oral corticosteroids were used for at least 6 weeks prior to study entry. The two control groups were 11 smokers with normal pulmonary function and 13 non-smokers. Airway resistance measurement using pulse oscillometric method. Nasal dry cold air is used to induce bronchoconstriction. Subjects were randomized to placebo (0.9% saline), a non-selective M blocker ipratropium bromide (500μg), a selective M_2 receptor agonist pilocarpine (5mg / ml) . The cold air is then induced to cause bronchoconstriction. Airway resistance after basal, preconditioning, and cold air challenge were measured and recorded.