The Use of the Internal Perimeter to Compare Airway Size and to Calculate Smooth Muscle Shortening

Hogg, James C.; Dunn, Lindsay; Paré, Peter D.

doi:10.1164/ajrccm/138.1.136

Cited by 209 publications

(145 citation statements)

References 13 publications

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“…In absolute terms, the amount of airway smooth muscle is lesser in the peripheral airways. A number of studies [8, 9, 15±17] have standardized the amount of smooth muscle in the airway wall by measuring the total cross-sectional area of smooth muscle seen on a transverse section of the airway and dividing it by the length of the basement membrane (the perimeter of the airway) since this is independent of the degree of airway smooth muscle contraction and lung inflation [18,19]. Expressing the amount of smooth muscle in this way, as mean thickness in relation to airway perimeter, allows a ready comparison between studies.…”

Section: Distribution Within Bronchial Treementioning

confidence: 99%

Airway smooth muscle in health and disease; methods of measurement and relation to function

James¹,

Carroll²

2000

Eur Respir J

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Smooth muscle is present and probably functional in the airways in utero and increases in absolute area during growth with little further change during adulthood. It encircles the entire airway below the level of the main bronchus, in a roughly circular orientation, except at high lung volumes. It occupies relatively more of the airway wall in the peripheral airways, reaching a maximum in the membranous bronchioles. Measurement of smooth muscle area in the airway wall is confounded by clinical classification of cases, methods of tissue retrieval and preparation, staining and orientation of sections, magnification, image analysis and statistical methods of comparison between groups. Airway smooth muscle area is pathologically increased in inflammatory conditions of the airways such as chronic obstructive pulmonary disease, in relation to airways obstruction, and asthma, in relation to severity and airway size (between 25 and 250% compared with control cases). It is increased in sudden infant death syndrome, but there are few studies in other conditions such as bronchiectasis. In asthma, smooth muscle must shorten (not necessarily to an abnormal degree) for the structural abnormalities of the airway to manifest as excessive airway narrowing. Not surprisingly there is renewed interest in the relationships between the mechanical and contractile properties of smooth muscle, parenchymal properties and lung volume and how these interact to determine smooth muscle length. The relative importance of smooth muscle area and mechanical properties, altered airway structure and airway inflammation in disease are yet to be determined.

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Section: Distribution Within Bronchial Treementioning

confidence: 99%

Airway smooth muscle in health and disease; methods of measurement and relation to function

James¹,

Carroll²

2000

Eur Respir J

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“…All other bronchi were classified according to their internal perimeter [19]: small bronchi (<1,000 mm), medium-sized bronchi (1,000±2,000 mm) and large bronchi (>2,000 mm). This classification method is based on the fact that even when internal and external areas are subject to change, e.g.…”

Section: Morphometrymentioning

confidence: 99%

“…all bronchi with internal perimeter larger than 1,000 mm, morphometry showed that no airway alterations had occurred in terms of airway wall thickness in either of the smoke exposed groups. Although the bronchi size classification on basis of internal perimeter [19] may have misclassified some severely obstructed medium-sized bronchi as "small bronchi" the cigarette smoke induced lesion clearly occurred essentially at the level of the small bronchi. Small bronchi wall thickness was significantly increased due to cigarette exposure (CS group in fig.…”

Section: Morphometrymentioning

confidence: 99%

N-acetylcysteine prevents cigarette smoke induced small airways alterations in rats

et al. 2000

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This study investigated the effect of cigarette smoke exposure and the potential protection N-acetylcysteine (NAC) in rat lungs.Forty-eight rats were exposed to cigarette smoke (CS) for 10 weeks, without (CS group) or with (CS+NAC group) oral intake of NAC 200 mg . rat -1 . day -1 , or to fresh air (Control). All rat lungs were assessed in terms of lung function, ventilation distribution (nitrogen, helium and sulphur hexafluoride phase III slopes), and morphometry (airway wall thickening of small, medium and large bronchi).The small bronchi, defined as the airways with an internal perimeter <1,000 mm showed significantly thicker airway walls in the CS than in the Control group. By contrast, no airway wall thickening was observed in the CS+NAC group with respect to Control. Except for decreased lung volumes and compliance in CS and CS+NAC groups, which were entirely attributable to smaller body weight gain, lung function was indistinguishable from Control. Phase III slopes were significantly increased only in the CS group.In conclusion, smoke-induced alterations in the rat lungs were reflected in wall thickening of the small bronchi and increased ventilation maldistribution. These smoke-induced morphometric and ventilation distribution alterations were prevented by N-acetylcysteine. Eur Respir J 2000; 15: 505±511. In humans, a major site of inflammatory action of cigarette smoke has been attributed to the so-called small airways, stimulating a number of studies aimed at characterizing and detecting structural change in the lung periphery [1,2]. The phase III slope of the N 2 single breath washout (SBW) test became a popular index of small airways alteration since the work by COSIO et al. [3] showed its correlation with morphological scores of small airways abnormalities in smokers with normal spirometry. A later SBW study by VAN MUYLEM et al. [4], which included helium and sulphur hexafluoride tracer concentrations, also revealed distinct correlations between indices derived from He and SF 6 slopes and airway pathology scores. Due to the fact that the diffusion front is located more peripherally for SF 6 than for He, the respective phase III slopes are indicative of the site where ventilation inhomogeneities occur.Although animal studies are well-suited for the study of lung function in the diseased lung, the difficulty often resides in reproducing a lesion which is comparable to that encountered in the human lung [5]. Previous studies in rats have led to conflicting results as to whether the cigarette smoke induces emphysematous lesions [6,7] or not [8,9] and not all studies provide any information about the extent to which the nonalveolated airways are affected [10]. Despite these difficulties, rat lungs have been used to investigate the possible protective role of N-acetylcysteine (NAC) over cigarette smoke induced lesions. NAC is an antioxidant and can therefore be expected to change lung oxidant-antioxidant imbalance induced by cigarette smoke which is a source of oxidants. Previous histopathology...

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“…Extraparenchymae airway walls were evaluated for the airway lumen, defined as the area circumscribed by the basement membrane of epithelium (LuB) and the outer border of the airway wall (Ae). The area of the airway wall (Aw) was calculated as the difference between Ae and LuB [11]. Airways whose ratio of maximal to minimal internal diameter were 5 2 were considered to be cut obliquely and were not measured.…”

Section: Data Analysesmentioning

confidence: 99%

Tissue-dependent differences in the asynchronous appearance of mast cells in normal mice and in congenic mast cell-deficient mice after infusion of normal bone marrow cells

Friend

Austen

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe time courses of the appearance of tissue mast cells in six sites were compared in normal WBB6F 1 -= As assessed by morphometric analysis of Carnoy's solution-fixed, methylene blue-stained tissue sections, the density of mast cells in the stomach mucosa, stomach submucosa, and spleen of = mice reached maximal levels by 8 weeks of age, whereas the density of mast cells in the skin, extraparenchymal airway walls, and lung parenchyma did not reach maximal levels until 18 weeks of age. When 8-week-old W = W v mice were infused with 2 2 10 7 bone marrow cells from = mice, mast cells appeared in the stomach mucosa and submucosa after 2 . 5 weeks, in the spleen and extraparenchymal airway walls after 5 weeks, and in the lung parenchyma after 10 weeks. Twenty weeks after bone marrow infusion, the mast cell densities in the spleen, stomach mucosa, and stomach submucosa were seven-, 13-, and five-fold greater, respectively, than those in age-matched = mice, but were eight-, two-, and fivefold lower in the skin, extraparenchymal airway walls, and lung parenchyma, respectively. Thus, those tissues that in =W v mice to assess mast cell dependency. Our results indicate that the capacity to restore a mast cell-dependent response in a particular tissue of the latter mice may relate to the local mast cell density and whether the immunological challenge activates mast cells only in that tissue or systematically with attendant widespread release of proinflammatory mediators.

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The Use of the Internal Perimeter to Compare Airway Size and to Calculate Smooth Muscle Shortening

Cited by 209 publications

References 13 publications

Airway smooth muscle in health and disease; methods of measurement and relation to function

Airway smooth muscle in health and disease; methods of measurement and relation to function

N-acetylcysteine prevents cigarette smoke induced small airways alterations in rats

Tissue-dependent differences in the asynchronous appearance of mast cells in normal mice and in congenic mast cell-deficient mice after infusion of normal bone marrow cells

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