Dybas Joseph M, Andresen Catharine J, Schelegle Edward S, McCue Ryan W, Callender Natasha N, Jackson Andrew C
Biomedical Engineering Dept., Boston Univ., 44 Cummington St., Boston, MA 02215, USA.
J Appl Physiol (1985). 2006 Mar;100(3):786-91. doi: 10.1152/japplphysiol.01014.2004.
Deep-breath frequency has been shown to increase in spontaneously obstructed asthmatic subjects. Furthermore, deep breaths are known to be regulated by lung rapidly adapting receptors, yet the mechanism by which these receptors are stimulated is unclear. This study tested the hypothesis that deep-breath frequency increases during experimentally induced bronchoconstriction, and the magnitude of the increased deep-breath frequency is dependent on the method by which bronchoconstriction is induced. Nine cynomolgus monkeys (Macaca fascicularis) were challenged with methacholine (MCh), Ascaris suum (AS), histamine, or an external mechanical resistance. Baseline (BL) and challenge deep-breath frequency were calculated from the number of deep breaths per trial period. Airway resistance (Raw) and tissue compliance (Cti), as well as tidal volume, respiratory rate, and minute ventilation, were analyzed for BL and challenged conditions. Transfer impedance measurements were fit with the DuBois model to determine the respiratory parameters (Raw and Cti). The flow at the airway opening was measured and analyzed on a breath-by-breath basis to obtain the ventilatory parameters (tidal volume, respiratory rate, and minute ventilation). Deep-breath frequency resulting from AS and histamine challenges [0.370 (SD 0.186) and 0.467 breaths/min (SD 0.216), respectively] was significantly increased compared with BL, MCh, or external resistance challenges [0.61 (SD 0.046), 0.156 (SD 0.173), and 0.117 breaths/min (SD 0.082), respectively]. MCh and external resistance challenges resulted in insignificant changes in deep-breath frequency compared with BL. All four modalities produced similar levels of bronchoconstriction, as assessed through changes in Raw and Cti, and had similar effects on the ventilatory parameters except that non-deep-breath tidal volume was decreased in AS and histamine. We propose that increased deep-breath frequency during AS and histamine challenge is the result of increased vascular permeability, which acts to increase rapidly adapting receptor activity.
研究表明,自发性气道阻塞的哮喘患者深呼吸频率会增加。此外,已知深呼吸受肺快速适应感受器调节,但其受刺激的机制尚不清楚。本研究检验了以下假设:实验性诱导支气管收缩期间深呼吸频率增加,且深呼吸频率增加的幅度取决于诱导支气管收缩的方法。对9只食蟹猴(猕猴)进行了乙酰甲胆碱(MCh)、猪蛔虫(AS)、组胺或外部机械阻力激发试验。根据每个试验期的深呼吸次数计算基线(BL)和激发后的深呼吸频率。分析了BL和激发试验条件下的气道阻力(Raw)、组织顺应性(Cti)以及潮气量、呼吸频率和分钟通气量。将传递阻抗测量值与杜波依斯模型拟合,以确定呼吸参数(Raw和Cti)。逐次测量并分析气道开口处的气流,以获得通气参数(潮气量、呼吸频率和分钟通气量)。与BL、MCh或外部阻力激发试验相比,AS和组胺激发试验导致的深呼吸频率显著增加[分别为0.370(标准差0.186)和0.467次/分钟(标准差0.216)],而BL、MCh或外部阻力激发试验的深呼吸频率分别为0.61(标准差0.046)、0.156(标准差0.173)和0.117次/分钟(标准差0.082)。与BL相比,MCh和外部阻力激发试验导致的深呼吸频率变化不显著。通过Raw和Cti的变化评估,所有四种激发方式产生的支气管收缩水平相似,对通气参数的影响也相似,只是AS和组胺激发试验中,非深呼吸潮气量减少。我们认为,AS和组胺激发试验期间深呼吸频率增加是血管通透性增加的结果,血管通透性增加会使快速适应感受器的活性增强。