Fujimori K, Satoh M, Arakawa M
Department of Medicine (II), Niigata University School of Medicine, Japan.
Chest. 1996 Jun;109(6):1525-31. doi: 10.1378/chest.109.6.1525.
Conflicting results from previous studies on the effect of bronchial challenge on ventilatory patterns in asthmatics may be due to airflow obstruction present before induction of bronchospasm onset, as well as the different degrees of bronchoconstriction induced.
We examined the ventilatory response to stepwise increments in respiratory resistance (Rrs) induced by continuous methacholine inhalation in eight patients with mild stable asthma without airway obstruction and eight normal subjects. Methacholine was inhaled continuously during tidal breathing until a nearly two-fold increase in Rrs was observed. Respiratory parameters, including tidal volume (VT), respiratory frequency (f), inspiratory ventilation (VI), mean inspiratory flow (VT/TI), and duty ratio (TI/TT), were measured simultaneously by respiratory inductive plethysmograph (RIP). Arterial oxygen saturation (SaO2) was examined by pulse oximetry. The end-tidal CO2 fraction (FETCO2) was measured with a rapid-response infrared analyzer at the mouthpiece.
Rrs, SaO2, FETCO2, and respiratory parameters, measured after saline solution inhalation, were not different between the two groups. Inhaled methacholine first decreased and then increased VI in both groups. However, changes in VI occurred earlier and to a greater extent in asthmatics than in normal subjects. At 200% Rrs (percent control), %VI was greater in asthmatics than in normal subjects (p<0.005) because of significant differences in %VT and %VT/TI between the two groups.
For a given degree of bronchoconstriction, the ventilatory response was more rapid and greater in patients with mild stable asthma without airway obstruction than in normal subjects. The different response to bronchial challenge between the two groups may be due to different increases in drive due to irritant receptor stimulation.
先前关于支气管激发对哮喘患者通气模式影响的研究结果相互矛盾,这可能是由于在支气管痉挛发作诱导前存在气流阻塞,以及诱导的支气管收缩程度不同所致。
我们研究了8例无气道阻塞的轻度稳定哮喘患者和8例正常受试者在持续吸入乙酰甲胆碱诱导呼吸阻力(Rrs)逐步增加时的通气反应。在潮式呼吸期间持续吸入乙酰甲胆碱,直至观察到Rrs增加近两倍。通过呼吸感应体积描记法(RIP)同时测量呼吸参数,包括潮气量(VT)、呼吸频率(f)、吸气通气量(VI)、平均吸气流量(VT/TI)和占空比(TI/TT)。通过脉搏血氧饱和度仪检测动脉血氧饱和度(SaO2)。在接口处用快速响应红外分析仪测量呼气末二氧化碳分数(FETCO2)。
两组在吸入盐水溶液后测量的Rrs、SaO2、FETCO2和呼吸参数无差异。两组吸入乙酰甲胆碱后VI均先降低后升高。然而,哮喘患者的VI变化比正常受试者更早且程度更大。在Rrs为200%(对照百分比)时,由于两组之间%VT和%VT/TI存在显著差异,哮喘患者的%VI高于正常受试者(p<0.005)。
对于给定程度的支气管收缩,无气道阻塞的轻度稳定哮喘患者的通气反应比正常受试者更快且更大。两组对支气管激发的不同反应可能是由于刺激感受器刺激导致驱动增加不同所致。