Slats Annelies M, Janssen Kirsten, de Jeu Ronald C, van der Plas Dirk T, Schot Robert, van den Aardweg Joost G, Sterk Peter J
Dept. of Pulmonology, Leiden Univ. Medical Center, PO Box 9600, NL-2300 RC, Leiden, The Netherlands.
J Appl Physiol (1985). 2008 Dec;105(6):1725-32. doi: 10.1152/japplphysiol.01237.2007. Epub 2008 Sep 18.
Deep inspiration temporarily reduces induced airways obstruction in healthy subjects. This bronchodilatory effect of deep inspiration is impaired in asthma. Passive machine-assisted lung inflation may augment bronchodilation compared with an active deep inspiration in patients with asthma by either opening closed airways or by reducing fluid flux across the airway wall during deep inspiration, and thereby increasing the tethering forces on the airway wall. We recruited 24 patients with asthma [18-46 yr old, forced expiratory volume in 1 s (FEV(1)) > 70% predicted; provocative concentration of methacholine inducing a 20% fall in FEV(1) (PC(20)) < 8 mg/ml], with either an impaired (n = 12) or an intact (n = 12) bronchodilatory response to deep inspiration. Two methacholine challenges were performed on separate days. At a 50% increase in respiratory resistance (forced oscillation technique at 8 Hz), the change in resistance by a positive-pressure inflation (computer-driven syringe) or an active deep inspiration was measured in randomized order. The reduction in resistance by positive-pressure inflation was significantly greater than by active deep inspiration in the impaired deep inspiration response group (mean change +/- SE: -0.6 +/- 0.1 vs. -0.03 +/- 0.2 cmH(2)O.l(-1).s, P = 0.002). No significant difference was found between positive-pressure inflation and active deep inspiration in the intact deep inspiration response group (-0.6 +/- 0.2 vs. -1.0 +/- 0.3 cmH(2)O.l(-1).s, P = 0.18). Positive-pressure inflation of the lungs can significantly enhance deep inspiration-induced bronchodilation in patients with asthma.
深吸气可暂时减轻健康受试者的诱发性气道阻塞。哮喘患者深吸气的这种支气管扩张作用受损。对于哮喘患者，与主动深吸气相比，被动机械辅助肺膨胀可能通过打开闭合气道或减少深吸气期间跨气道壁的液体通量，从而增加气道壁上的牵拉力，进而增强支气管扩张作用。我们招募了24例哮喘患者[年龄18 - 46岁，1秒用力呼气容积(FEV₁)>预计值的70%；引起FEV₁下降20%的乙酰甲胆碱激发浓度(PC₂₀)<8 mg/ml]，其中对深吸气的支气管扩张反应受损的患者12例，反应正常的患者12例。在不同日期进行两次乙酰甲胆碱激发试验。在呼吸阻力增加50%时(8 Hz强迫振荡技术)，以随机顺序测量正压通气(计算机驱动注射器)或主动深吸气引起的阻力变化。在深吸气反应受损组中，正压通气引起的阻力降低显著大于主动深吸气(平均变化±标准误：-0.6±0.1 vs. -0.03±0.2 cmH₂O·l⁻¹·s，P = 0.002)。在深吸气反应正常组中，正压通气与主动深吸气之间未发现显著差异(-0.6±0.2 vs. -1.0±0.3 cmH₂O·l⁻¹·s，P = 0.18)。对哮喘患者进行肺正压通气可显著增强深吸气诱导的支气管扩张作用。
