Thorpe C William, Salome Cheryl M, Berend Norbert, King Gregory G
Woolcock Institute of Medical Research, Camperdown, NSW 2050, Australia.
J Appl Physiol (1985). 2004 Nov;97(5):1643-53. doi: 10.1152/japplphysiol.01300.2003. Epub 2004 Jul 16.
Using the forced oscillation technique, we tracked airway resistance continuously during quiet breathing (QB) and deep inspiration (DI), thus observing fluctuations in resistance that may reflect mechanisms of airway stretch and renarrowing. After DI, however, the resistance may be depressed for a period not related to volume changes. We hypothesized that this gradual increase in resistance after DI-induced dilation was determined by a simple time constant. Furthermore, to the extent that this effect reflects dynamic characteristics of airway renarrowing, the resistance change after each tidal inspiration should also be constrained by this temporal limit. A model relating resistance fluctuations to the breathing pattern, including both instantaneous and delayed effects, was developed and applied to data from 14 nonasthmatic and 17 asthmatic subjects (forced expiratory volume in 1 s = 103 +/- 13 and 83 +/- 12%, respectively, means +/- SD) after methacholine challenge (dose 145 +/- 80 and 3.0 +/- 3.4 micromol, respectively) that resulted in respective forced expiratory volume in 1 s reductions of 16 +/- 7 and 24 +/- 6% from baseline. Resistance was measured continuously for 1 min of QB, a DI, followed by a further minute of QB. Resistance values at end expiration (Ree) and end inspiration were calculated. We found that the sequence of Ree after DI was best modeled by a power-law function of time rather than an exponential decay (r2 = 0.82 +/- 0.18 compared with 0.63 +/- 0.16; P < 0.01). Furthermore, the coefficient characterizing this "renarrowing function" was close to equal to the coefficient characterizing the equivalent function of resistance change between each resistance value at end inpiration and subsequent Ree during QB, particularly in the nonasthmatic subjects for whom the intraclass correlation was 0.66. This suggests that the same time-dependent factors determine renarrowing after both large and small breaths.
我们使用强迫振荡技术,在安静呼吸(QB)和深吸气(DI)过程中持续追踪气道阻力,从而观察到阻力的波动,这些波动可能反映了气道伸展和再变窄的机制。然而,在深吸气后,阻力可能会在一段与容积变化无关的时间内降低。我们假设,深吸气诱导扩张后阻力的这种逐渐增加是由一个简单的时间常数决定的。此外,就这种效应反映气道再变窄的动态特征而言,每次潮气量吸气后的阻力变化也应受此时间限制的约束。我们建立了一个将阻力波动与呼吸模式相关联的模型,该模型包括即时和延迟效应,并将其应用于14名非哮喘患者和17名哮喘患者(一秒用力呼气量分别为103±13%和83±12%,均值±标准差)在乙酰甲胆碱激发试验(剂量分别为145±80和3.0±3.4微摩尔)后的数据,激发试验导致一秒用力呼气量相对于基线分别降低了16±7%和24±6%。在安静呼吸1分钟、一次深吸气,随后再进行1分钟安静呼吸的过程中持续测量阻力。计算呼气末(Ree)和吸气末的阻力值。我们发现,深吸气后Ree的序列最好用时间的幂律函数而非指数衰减来建模(r2 = 0.82±0.18,而指数衰减为0.63±0.16;P < 0.01)。此外,表征这种“再变窄函数”的系数接近于表征安静呼吸期间吸气末每个阻力值与随后Ree之间阻力变化等效函数的系数,特别是在组内相关性为0.66的非哮喘患者中。这表明,无论呼吸幅度大小,相同的时间依赖性因素决定了再变窄过程。