Airway muscle stereology: implications for increased shortening in asthma.
Airway muscle stereology: implications for increased shortening in asthma.
复制标题
气道肌肉立体学：对哮喘缩短增加的影响。
DOI：
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发表时间：
1996
影响因子：
24.7
通讯作者：
R R Schellenberg
中科院分区：
文献类型：
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作者：
R. Thomson;A M Bramley;R R Schellenberg
尽管迄今为止的研究存在许多方法学局限性，但由于增生或肥大而导致的气道平滑肌增加被认为是哮喘中支气管过度收缩的原因。我们最近未能证明哮喘气道准备中肌肉体积的增加与非哮喘对照相比缩短了 3 倍，这促使我们重新评估哮喘气道与非哮喘气道中的肌肉数量。使用标准化体视学方法对来自五名哮喘受试者和五名非哮喘吸烟者的组织中横截面气道平滑肌轮廓的高放大图像，对轴向切片的第二代至第四代支气管中的平滑肌进行量化。当数据按总横截面组织面积标准化时，两组（哮喘组与非哮喘组）之间的平滑肌比例（3.45 +/- 0.81% 与 2.74 +/- 0.76%）、肌细胞之间的细胞外基质（1.65 +/- 0.46% 与 1.06 +/- 0.25%）或平滑肌束内结缔组织（1.65）的比例没有差异。 +/- 0.34% 与 1.53 +/- 0.59%）。这些用于以高分辨率评估轴向气道切片中的横截面气道肌肉的方法没有提供哮喘大气道中气道平滑肌增加的证据，并且表明哮喘气道的机械反应的差异不能仅用平滑肌的量来解释。
Increased airway smooth muscle, resulting from either hyperplasia or hypertrophy, has been implicated as a cause of excessive bronchoconstriction in asthma despite the many methodologic limitations of studies to date. Our recent failure to demonstrate increased muscle volume in an asthmatic airway preparation having 3-fold greater shortening than nonasthmatic controls prompted us to reassess the quantity of muscle in asthmatic versus nonasthmatic airways. Smooth muscle was quantified in axially sectioned, 2nd- to 4th-generation bronchi, using standardized stereologic methods on high-magnification images of cross-sectional airway smooth muscle profiles in tissues from five asthmatic subjects and five nonasthmatic smokers. When data were normalized by total cross-sectional tissue area, no differences between the two groups (asthmatic versus nonasthmatic) were detected for the proportion of smooth muscle (3.45 +/- 0.81% versus 2.74 +/- 0.76%), extracellular matrix between muscle cells (1.65 +/- 0.46% versus 1.06 +/- 0.25%), or connective tissue within smooth muscle bundles (1.65 +/- 0.34% versus 1.53 +/- 0.59%). These methodologies for evaluating cross-sectional airway muscle in axial airway sections at high resolution provide no evidence of increased airway smooth muscle in asthmatic large airways, and suggest that differences in mechanical responses of asthmatic airways cannot be explained solely by the amount of smooth muscle.