背景:增加功能性残余容量(FRC)或潮气量(VT)降低了气道阻力,并减弱了动物和人类对支气管收缩刺激的反应。未知的是上述机制中的哪一种在调节气道口径方面更有效,以及它们的组合是否产生累加或协同作用。为了解决这个问题,我们研究了FRC增加和VT增加对缓解健康人吸入乙酰甲胆碱(MCh)诱导的支气管收缩的影响.
方法:19名健康志愿者接受单剂量MCh的攻击,并使用强制振荡测量5和19Hz(R5和R19)的吸气阻力,它们的差异(R5-19),在自主呼吸期间和在FRC增加的情况下施加的呼吸模式期间,以及在5Hz(X5)的电抗,或VT,或者两者兼而有之。重要的是,在我们的实验设计中,我们保持了VT和呼吸频率(BF)的乘积,即,分钟通气(VE)固定,以更好地隔离室性心动过速变化的影响。
结果:从基线FRC开始的三倍VT显着减弱了MCh对R5,R19,R5-19和X5的影响。VT加倍而BF减半的影响不大。通过一个或两个VT增加FRC显著减弱MCh对R5、R19、R5-19和X5的影响。增加VT和FRC对R5,R19,R5-19和X5具有累加作用,但增加FRC的作用比增加VT的作用更一致,因此表明更大的支气管扩张。当在等体积下比较时,除了室性心动过速是自主呼吸时的三倍外,呼吸模式之间没有差异.
结论:这些数据表明,增加FRC和VT可以通过累加效应减弱健康人诱导的支气管收缩,这些效应主要与平均手术肺容量增加有关。我们建议在恒定VE下,随着FRC的增加,静态拉伸比潮汐拉伸更有效,可能是通过对气道几何形状和气道平滑肌动力学的综合影响。
BACKGROUND: Increasing functional residual capacity (FRC) or tidal volume (VT) reduces airway resistance and attenuates the response to bronchoconstrictor stimuli in animals and humans. What is unknown is which one of the above mechanisms is more effective in modulating airway caliber and whether their combination yields additive or synergistic effects. To address this question, we investigated the effects of increased FRC and increased VT in attenuating the
bronchoconstriction induced by inhaled methacholine (MCh) in healthy humans.
METHODS: Nineteen healthy volunteers were challenged with a single-dose of MCh and forced oscillation was used to measure inspiratory resistance at 5 and 19 Hz (R5 and R19), their difference (R5-19), and reactance at 5 Hz (X5) during spontaneous breathing and during imposed breathing patterns with increased FRC, or VT, or both. Importantly, in our experimental design we held the product of VT and breathing frequency (BF), i.e, minute ventilation (VE) fixed so as to better isolate the effects of changes in VT alone.
RESULTS: Tripling VT from baseline FRC significantly attenuated the effects of MCh on R5, R19, R5-19 and X5. Doubling VT while halving BF had insignificant effects. Increasing FRC by either one or two VT significantly attenuated the effects of MCh on R5, R19, R5-19 and X5. Increasing both VT and FRC had additive effects on R5, R19, R5-19 and X5, but the effect of increasing FRC was more consistent than increasing VT thus suggesting larger bronchodilation. When compared at iso-volume, there were no differences among breathing patterns with the exception of when VT was three times larger than during spontaneous breathing.
CONCLUSIONS: These data show that increasing FRC and VT can attenuate induced
bronchoconstriction in healthy humans by additive effects that are mainly related to an increase of mean operational lung volume. We suggest that static stretching as with increasing FRC is more effective than tidal stretching at constant VE, possibly through a combination of effects on airway geometry and airway smooth muscle dynamics.