Are all airways equal?
Are all airways equal?
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所有航空公司都平等吗？
DOI：
10.1152/japplphysiol.00253.2012
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发表时间：
2012
期刊：
影响因子：
--
通讯作者：
Venegas,JoseG
中科院分区：
文献类型：
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作者：
Winkler,Tilo;Venegas,JoseG
支气管收缩是哮喘的主要特征。它涉及气道狭窄，气道阻力增加，呼吸障碍，在非常严重的情况下甚至会导致死亡。支气管收缩期间气道腔的严重狭窄是由气道平滑肌响应于激动剂或迷走神经刺激而缩短引起的。然而，在离体气道或组织条中容易观察到的简单刺激-反应关系在体内是否同样适用于所有气道？二十多年前，研究人员使用多种惰性气体消除技术（MIGET）表明，哮喘的支气管收缩导致不均匀的通气-灌注分布（2）。这表明整个支气管树的气道管腔狭窄一定是高度异质性的，从而导致与哮喘中测量的通气-灌注分布一致的通气异质性。然而，尚不清楚支气管收缩的这种异质性是由气道反应的随机变异性引起的，因此在肺内随机分布，还是主要位于肺的相邻区域。在过去十年中，使用PET、MRI和同步加速器CT进行的肺部成像研究发现，支气管收缩导致以大面积通气缺陷（VDefs）为特征的大量斑片状模式，例如，参考文献1、4、7、8、10-12。这些结果与在大中心气道（大约五代气道）中使用CT进行的气道管腔面积的体内测量结果形成对比，该测量结果未能显示解释在大VDEF中观察到的通气不足所需的收缩。综上所述，这些发现表明室间隔缺损的主要原因是较小气道的收缩（12）。
BRONCHOCONSTRICTION IS A CARDINAL feature of asthma. It involves airway narrowing, increase in airway resistance, impairment of breathing, and can in very severe cases even lead to death. The severe narrowing of the airway lumen during bronchoconstriction is caused by a shortening of the airway smooth muscle in response to agonists or vagal stimulation. However, does a simple stimulus-response relationship, easily observed in isolated airways or tissue strips, apply in vivo equally to all airways?More than two decades ago, investigators using the multiple inert gas elimination technique (MIGET) showed that bronchoconstriction in asthma resulted in inhomogeneous ventilation-perfusion distributions (2). That suggested that airway lumen narrowing throughout the bronchial tree must have been highly heterogeneous to cause the heterogeneity in ventilation consistent with the measured ventilation-perfusion distributions in asthma. However, it was unclear if such heterogeneity in bronchoconstriction was caused by a random variability in the response of airways and, thus, randomly distributed within the lungs, or if it was predominantly located in contiguous regions of the lungs. During the last decade, pulmonary imaging studies using PET, MRI, and synchrotron CT, found that bronchoconstriction leads to substantial patchy patterns characterized by large areas of ventilation defects (VDefs), eg, Ref. 1, 4, 7, 8, 10–12. Those results contrasted with in vivo measurements of airway luminal area with CT in large central airways (approximately five airway generations), which failed to show the constriction needed to explain the hypoventilation seen in large VDefs. Taken together, these findings suggested that the primary cause of VDefs was the constriction of smaller airways (12).