Pathophysiology of Pertpheral Airways in Chronic Obstructive Pulmonary Disease

摘要通过观察呼吸阻力（Rrs）和解剖死亡间隙（V_D），探讨稳定型和自发性哮喘患者对阿托品和非诺特罗气雾剂以及静脉注射氨茶碱的气道反应的有效部位。以V_D评价中心气道反应，以Rrs评价总反应。当V_D变化轻微时，通过Rrs推断外周气道反应。潮汐呼吸时连续吸入阿托品（4mg /m1）或非诺特罗（0.4 mg/ml） 5min。在稳定型哮喘和自发性哮喘患者中，同时吸入阿托品和非诺特罗可增加Grs （Rrs的互比）（p|0.01），同时增加V_D （p|0.01）。非诺特罗增加自发性哮喘患者Grs的作用大于阿托品，其V_D的增加与之相当（p < 0.05）。静脉注射氨茶碱（250 mg）对稳定型哮喘患者的Grs和V_D均无影响，而自发性哮喘患者的Grs明显升高（P < 0.01）， V_D无变化。上述结果提示，吸入阿托品诱导支气管扩张的主要部位为中央气道，静脉注射氨茶碱诱导支气管扩张的主要部位为外周气道，而吸入非诺特罗对哮喘患者的中央和外周气道均有扩张作用。在支气管哮喘的治疗中，临床使用的支气管扩张剂在有效部位上的差异可以被考虑。

AbstractWe studied the effective sites of airway response to atropine and fenoterol aerosols and to the intravenous injection of aminophylline in patients with stable and spontaneous asthma, by the simultaneous assessment of respiratory resistance (Rrs) and anatomic dead space (V_D). Central airway response was determined by V_D, and overall response was determined by Rrs. Peripheral airway response was inferred from Rrs when the change in V_D was slight. Atropine (4 mg/m1) or fenoterol (0.4 mg/ml) was continously inhaled during tidal breathing for 5 min. Inhalation of both atropine and fenoterol increased Grs (reciprocal of Rrs) (p|0.01) with a simultaneous increase in V_D (P|0.01) in the patients with stable and spontaneous asthma. Fenoterol increased Grs more than did atropine at an equivalent increase in V_D in patients with spontaneous asthma (p|0.05). Intravenous injection of aminophylline (250 mg) had no effects on either Grs or V_D in patients with stable asthma, but it significantly increased Grs (P|0.01) without change in V_D in patients with spontaneous asthma. These results suggest that the predominant sites of bronchodilation induced by inhaled atropine are the central airways, and those induced by intravenous injection of aminophylline are the peripheral airways, and that inhaled fenoterol dilates both the central and peripheral airways in asthmatic subjects. Differences among clinically used bronchodilators on the effective sites may be considered in the treatment of bronchial asthma.