Bronchodilation response to deep inspirations in asthma is dependent on airway distensibility and air trapping.
Bronchodilation response to deep inspirations in asthma is dependent on airway distensibility and air trapping.
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DOI：
10.1152/japplphysiol.00603.2010
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发表时间：
2011-02
影响因子：
3.3
通讯作者：
G. Pyrgos;N. Scichilone;A. Togias;Robert H. Brown
中科院分区：
文献类型：
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作者：
G. Pyrgos;N. Scichilone;A. Togias;Robert H. Brown
在健康个体中，深度吸气（DIs）对甲胆碱（MCh）诱导的支气管收缩具有有效的支气管扩张能力。这在哮喘中有不同程度的减弱。我们假设DIs患者支气管不能扩张与气道扩张性降低有关。我们研究了15例基线肺功能范围较宽的哮喘患者（1 s内强迫呼气容积(FEV(1)) =预测值的60-99%）的di诱导支气管扩张与气道扩张之间的关系。受试者停止吸入吸入20分钟后，接受单剂量MCh刺激，然后要求进行吸入吸入。通过受试者改善FEV的能力来评估吸入吸入的有效性(1)。通过两组高分辨率CT扫描对同一受试者进行研究，一组是功能剩余容量（FRC），另一组是总肺容量（TLC）。在每个受试者中，匹配并测量21-41个气道（FRC时直径0.8-6.8 mm）的面积，计算气道扩张率（从FRC到TLC时气道直径的增加）。FEV(1) <75%预测组DIs的支气管扩张能力显著低于FEV(1)≥75%预测组（15±11% vs. 46±9%,P = 0.04），且与气道扩张率（r = 0.57, P = 0.03）、残气量(RV)/TLC （r = -0.63, P = 0.01）密切相关。在多元回归中，只有RV/TLC是di诱导的支气管扩张的重要决定因素。当使用沙丁胺醇进行最大支气管扩张后检查气道时，这些关系消失了。我们的数据表明，DI在哮喘中支气管扩张作用的丧失与肺膨胀扩张气道的能力有关，这反过来又与空气捕获的程度和气道平滑肌张力有关。这些关系仅存在于气道张力存在的情况下，表明高分辨率CT显示的传导气道的结构变化并不起关键作用。
In healthy individuals, deep inspirations (DIs) have a potent bronchodilatory ability against methacholine (MCh)-induced bronchoconstriction. This is variably attenuated in asthma. We hypothesized that inability to bronchodilate with DIs is related to reduced airway distensibility. We examined the relationship between DI-induced bronchodilation and airway distensibility in 15 asthmatic individuals with a wide range of baseline lung function [forced expired volume in 1 s (FEV(1)) = 60-99% predicted]. After abstaining from DIs for 20 min, subjects received a single-dose MCh challenge and then asked to perform DIs. The effectiveness of DIs was assessed by the ability of the subjects to improve FEV(1). The same subjects were studied by two sets of high-resolution CT scans, one at functional residual capacity (FRC) and one at total lung capacity (TLC). In each subject, the areas of 21-41 airways (0.8-6.8 mm diameter at FRC) were matched and measured, and airway distensibility (increase in airway diameter from FRC to TLC) was calculated. The bronchodilatory ability of DIs was significantly lower in individuals with FEV(1) <75% predicted than in those with FEV(1) ≥75% predicted (15 ± 11% vs. 46 ± 9%, P = 0.04) and strongly correlated with airway distensibility (r = 0.57, P = 0.03), but also with residual volume (RV)/TLC (r = -0.63, P = 0.01). In multiple regression, only RV/TLC was a significant determinant of DI-induced bronchodilation. These relationships were lost when the airways were examined after maximal bronchodilation with albuterol. Our data indicate that the loss of the bronchodilatory effect of DI in asthma is related to the ability to distend the airways with lung inflation, which is, in turn, related to the extent of air trapping and airway smooth muscle tone. These relationships only exist in the presence of airway tone, indicating that structural changes in the conducting airways visualized by high-resolution CT do not play a pivotal role.