THE STRUCTURE OF LARGE AND SMALL AIRWAYS IN NONFATAL AND FATAL ASTHMA

THE STRUCTURE OF LARGE AND SMALL AIRWAYS IN NONFATAL AND FATAL ASTHMA
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DOI:
10.1164/ajrccm/147.2.405
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发表时间:
1993-02-01
期刊:
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子:
--
通讯作者:
JAMES, A
JAMES, A
中科院分区:
其他
文献类型:
--
作者:
CARROLL, N;ELLIOT, J;JAMES, A

文献摘要

被引文献

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哮喘的特征是过度的气道狭窄和气道壁炎症。在致命性哮喘的病例中,可以观察到气道壁厚度的增加,这可能是当平滑肌收缩时气道壁过度狭窄的原因。这项研究是为了检查致命性和非致命性哮喘病例中大小呼吸道的大小。比较哮喘死亡组(致死性哮喘组,n=11)、非呼吸系统疾病猝死组(非致死性哮喘组,n=13)和无呼吸道病史组(对照组,n=11)大、小气道横断面的气道壁面积(相对于平滑肌层的总面积、内面积、外面积)、上皮完整性、平滑肌、软骨和粘液腺面积。使用基底膜周长按大小对气道进行分组以供比较。所有面积均以每毫米基底膜面积表示。致死性哮喘患者的软骨性呼吸道总壁、内壁、外壁、平滑肌、粘液腺和软骨面积均大于对照组和非致死组。致死性和非致死性病例的内壁面积均大于对照组(P<0.05)。在小MB(周长2 mm)中,致死性和非致死性哮喘患者的总面积和外壁面积比对照组大(p<0.05)。在大MB(周长2~4 mm)中,致死性和非致命性哮喘患者的平滑肌面积均大于对照组(p<0.05),但致死性和非致命性哮喘患者之间的差异无统计学意义。不同病例间的平滑肌缩短和上皮破坏差异很大,但在大或小呼吸道的组间无显著差异。结论:致死性哮喘大、小气道均可发生结构改变,但非致死性哮喘主要发生在小气道。这些变化在广泛传播时,是容易死于哮喘还是由更严重的疾病导致,目前尚不清楚。
Asthma is characterized by excessive airway narrowing and airway wall inflammation. In cases of fatal asthma, increased thickness of the airway wall is observed and may account for excessive airway narrowing when smooth muscle contracts. This study was undertaken to examine airway dimensions in large and small airways in both fatal and nonfatal cases of asthma. Airway wall areas (total, inner, and outer relative to smooth muscle layer), epithelial integrity, smooth muscle shortening, and the areas of smooth muscle, cartilage, and mucous glands were compared in transverse sections of large and small airways of subjects dying of asthma (fatal asthma, n = 11), those dying suddenly of nonrespiratory diseases and having a definite history of asthma (nonfatal asthma, n = 13), and those dying suddenly without any history of respiratory illness (control, n = 11). Airways were grouped by size using the basement membrane perimeter for comparison. All areas were expressed as areas per millimeter of basement membrane. In cartilaginous airways, the cases of fatal asthma had greater (p < 0.05) total wall, inner wall, outer wall, smooth muscle, mucous gland and cartilage areas than did control and nonfatal cases. The inner wall area was greater in the fatal and nonfatal cases than in the control cases (p < 0.05) in the small cartilaginous airways and membranous bronchioles (MB). In small MB (perimeter < 2 mm), the total and outer wall areas were greater (p < 0.05) in cases of fatal and nonfatal asthma than in control cases. In large MB (perimeter, 2 to 4 mm), the area of smooth muscle was greater in fatal and nonfatal cases than in control cases (p < 0.05), but there were no differences between fatal and nonfatal cases of asthma. Smooth muscle shortening and epithelial disruption varied greatly between cases, but there were no significant differences between groups in large or small airways. It is concluded that structural changes that may increase airway responsiveness occur in large and small airways in fatal asthma, but they occur predominantly in the small airways in nonfatal cases of asthma. Whether these changes, when widespread, predispose to death from asthma or result from more severe disease is unknown.