Mechanisms involved in airway obstruction: the role of smooth muscle
Mechanisms involved in airway obstruction: the role of smooth muscle
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DOI：
10.1034/j.1398-9995.2000.00507.x
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发表时间：
2000-01-01
期刊：
影响因子：
12.4
通讯作者：
Scano, G
中科院分区：
文献类型：
--
作者：
Mazzarella, G;Stendardi, L;Scano, G
气道壁的结构变化可能是由慢性变态反应性炎症释放的介质推动的，这是哮喘的显著特征。然而，目前还不清楚发生在气道壁上的许多变化是如何导致哮喘患者气道功能改变的。在上皮下基质中的胶原沉积，在平滑肌周围和内部，预计将与平滑肌肉收缩的效果相反。相反，几何因素会导致给定程度的平滑肌缩短时，气道狭窄加剧；当给定的力由平滑肌产生时，气道壁的僵硬程度降低，而气道狭窄加剧。基质的降解可能会改变肌肉和肺反冲之间的耦合，从而允许过度的平滑肌肉缩短。与其收缩能力保持相关的肌肉质量的增加可能是导致气道过度狭窄的最重要因素。
Structural changes in the airway walls that are probably driven by mediators released as a consequence of chronic allergic inflammation are prominent features of asthma. However, it is not clear how each of the many changes that occur in the airway wall contribute to altered airway function in asthma. Collagen deposition in the subepithelial matrix, around and inside the smooth muscle, would be expected to oppose the effect of smooth-muscle contraction. Conversely, geometric factors would result in exaggerated airway narrowing for a given degree of smooth-muscle shortening; decreased airway wall stiffness and increased airway narrowing for a given amount of force generated by the smooth muscle. Degradation of the matrix may alter the coupling between muscle and lung recoil, allowing exaggerated smooth-muscle shortening. Increase in muscle mass associated with preservation of its contractile capacity could be the most important contributor to exaggerated airway narrowing.