Partitioning of pulmonary impedance in excised human and canine lungs

Brabandt, H Van; Cauberghs, M.; Verbeken, Eric; Moerman, Philippe; Lauweryns, Joseph M.; Woestijne, K. P. Van de

doi:10.1152/jappl.1983.55.6.1733

Cited by 97 publications

(62 citation statements)

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“…More importantly, the correlation coefficients between both airway parameters and FEV 1 (% predicted) improved as the airway size decreased from the third to the sixth generation both in B1 and B8. These results clearly support the concept that distal (small) airways rather than proximal (large) airways are the more important determinant of airflow limitation in COPD, as has been previously suggested by a number of pathology-function correlation studies in the past (11)(12)(13)(14).…”

Section: Discussionsupporting

confidence: 88%

“…Nakano and colleagues were the first to report that wall thickening at B1 in the right upper lobe had a significant correlation with FEV 1 (% predicted) (27), and they subsequently demonstrated that measuring airway dimensions in large airways could roughly estimate small airway dimensions by comparing the CT findings of large airways with the histologic measurement of small airways in lungs excised from the same subjects (28). The important role of small airway lesions in COPD airflow limitation has been long recognized (11)(12)(13)(14). In an earlier study, Hogg and colleagues used a retrograde catheter technique and were the first to report that the resistance in small airways of excised lungs from patients with COPD was greatly increased compared with normal lungs, in which 25% of the total airway resistance is accounted for by the small airways (11).…”

Section: Discussionmentioning

confidence: 99%

“…Thin-section computed tomography (CT) has been used to quantify emphysema by detecting low attenuation areas (LAA), and the role of CT in diagnosing emphysema, including subclinical emphysema (2,3), has been well established (4)(5)(6)(7)(8)(9). However, airflow limitation evaluated by forced expiratory volume in 1 s (FEV 1 ) does not necessarily have a good correlation with the severity of emphysema as evaluated by CT (10), because small airway disease appears to contribute more significantly to the airflow limitation in COPD (1,(11)(12)(13)(14).…”

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confidence: 99%

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Airflow Limitation and Airway Dimensions in Chronic Obstructive Pulmonary Disease

Hasegawa

Nasuhara

Onodera

et al. 2006

Am J Respir Crit Care Med

369

352

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Rationale: Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation caused by emphysema and/or airway narrowing. Computed tomography has been widely used to assess emphysema severity, but less attention has been paid to the assessment of airway disease using computed tomography. Conclusions:We are the first to use three-dimensional computed tomography to demonstrate that airflow limitation in COPD is more closely related to the dimensions of the distal (small) airways than proximal (large) airways.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Airflow Limitation and Airway Dimensions in Chronic Obstructive Pulmonary Disease

Hasegawa

Nasuhara

Onodera

et al. 2006

Am J Respir Crit Care Med

369

352

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“…These results were challenged by VAN BRABANDT et al [10]. They repeated the experiments of HOGG et al [7] described above, in normal lungs and compared the results to those in lungs with chronic obstructive disease.…”

Section: Animal and In Vitro Studiesmentioning

confidence: 98%

The distal airways: are they important in asthma?

Kraft¹

1999

Eur Respir J

131

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Although the airways of <2 mm in diameter have been dubbed the "quiet zone", they do not appear to be so in asthma. Physiological and pathological evidence suggests that the small airways and lung parenchyma participate in asthma pathogenesis, and may explain many of the clinical observations noted.This review presents this evidence, beginning with physiological evidence, followed by pathology and last by imaging studies that evaluate the distal lung. Seminal physiological studies date back to the 1960s, with significant progress in the area of airway smooth muscle and its contribution to airways responsiveness noted over the last several years.The use of bronchoscopy in clinical studies has complemented the autopsy studies in advancing knowledge about airway structural changes appreciated in asthma in the small airways and lung parenchyma. These pathological studies have allowed validation of the physiological, and more recently the imaging studies performed to evaluate this compartment of the lung in asthma.Thus, the evidence suggests that the small airways and parenchyma contribute significantly to asthma pathogenesis. The challenge now lies in evaluating this compartment in the context of its value as a therapeutic target in asthma. Eur Respir J 1999; 14: 1403±1417. Data from the last three decades have suggested that the distal lung, which includes the airways of <2 mm and the lung parenchyma, contributes to asthma pathogenesis. Due to the challenges raised in evaluating this part of the lung, this region has not been studied in the same level of detail as have the larger airways. However, a significant amount of pathological data from autopsy specimens and recently from chronic, stable asthmatics, evaluating the small airways and lung parenchyma, are available. These data, combined with physiological data, support a significant role for the distal lung as a contributor to airway inflammation and hyperresponsiveness. The following review will present this evidence and explore the clinically important issue of the distal lung as a therapeutic target in asthma. Physiology of the distal airways Animal and in vitro studiesThe small airways of <2 mm in diameter are pathways of low resistance, and normally contribute~10% of the total resistance to flow. These observations were made in, seminal contributions by MACKLEM and MEAD [1, 2] using a retrograde catheter technique. Using excised dog lobes, they placed a catheter containing bell shaped polyethylene tubing at one end. The bell was wedged into a bronchus with the catheter extending peripherally through the parenchyma and pleura. They showed that the peripheral resistance (Rp) was too small to detect at >80% of vital capacity (VC), but increased at lower volumes to 15% of the total lung resistance at 1% of VC. These data are in keeping with WEIBEL [3], who demonstrated that the cross-sectional area of the small airways was significantly larger than that of the central airways. BROWN et al. [4] further evaluated the effects of small airways occlusion...

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“…Although both McLean (2) and Leopold and Gough (3) believed that disease in the terminal and preterminal bronchioles preceded emphysematous destruction of respiratory bronchioles to form centrilobular emphysematous lesions in COPD, only Leopold and Gough conducted the three-dimensional reconstructions of the histology required to establish that 60% (54/90) of the 90 centrilobular lesions they examined by this method were supplied by bronchioles that had thickened walls and narrowed lumens (3). Subsequent reports established that the smaller bronchi and bronchioles less than 2 mm in diameter became the major site of airways obstruction in COPD (4)(5)(6), and a series of studies reviewed by Hogg and Timens (7) have confirmed and extended the original observations that these airways are chronically inflamed and extensively remodeled in COPD. Moreover, a multivariate analysis performed in a study of lung tissue from patients treated for advanced emphysema by lung volume reduction surgery has shown that thickening of the walls of the smaller bronchi and bronchioles by connective tissue and the accumulation of inflammatory exudates containing mucus explained more of the variance in the decline of FEV 1 than the infiltration by any particular inflammatory cell type (8).…”

mentioning

confidence: 99%

Differential Expression of Tissue Repair Genes in the Pathogenesis of Chronic Obstructive Pulmonary Disease

Gosselink

Hayashi

Elliott

et al. 2010

Am J Respir Crit Care Med

132

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Rationale: The airflow limitation that defines severity of chronic obstructive pulmonary disease (COPD) is caused by a combination of small airway obstruction and emphysematous lung destruction. Objectives: To examine the hypothesis that small airway obstructive and emphysematous destructive lesions are produced by differential expression of genes associated with tissue repair. Methods: The expression of 54 genes associated with repair of repetitively damaged tissue was measured in 136 paired samples of small bronchioles and surrounding lung tissue separated by laser capture microdissection. These samples were collected from 63 patients at different levels of disease severity who required surgery for either lung cancer or lung transplantation for very severe COPD. Gene expression was measured by quantitative polymerase chain reaction in these paired samples and compared with the FEV 1 by linear regression analysis. Measurements and Main Results: After corrections for false discovery rates, only 2 of 10 genes (serpin peptidase inhibitor/plasminogen activator inhibitor member 2 and matrix metalloproteinase [MMP] 10) increased, whereas 8 (MMP2, integrin-a1, vascular endothelial growth factor, a disintegrin and metallopeptidase domain 33, scatter factor/hepatocyte growth factor, tissue inhibitor of matrix metalloproteinase-2, fibronectin, and collagen 3a1) decreased in small airways in association with FEV 1 . In contrast, 8/12 genes (early growth response factor 1, MMP1, MMP9, MMP10, plasminogen activator urokinase, plasminogen activator urokinase receptor, tumor necrosis factor, and IL13) increased and 4/12 (MMP2, tissue inhibitor of matrix metalloproteinase-1, collagen 1a1, and transforming growth factor-b3) decreased in the surrounding lung tissue in association with progression of COPD. Conclusions: The progression of COPD is associated with the differential expression of a cluster of genes that favor the degradation of the tissue surrounding the small conducting airways.

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Partitioning of pulmonary impedance in excised human and canine lungs

Cited by 97 publications

References 0 publications

Airflow Limitation and Airway Dimensions in Chronic Obstructive Pulmonary Disease

Airflow Limitation and Airway Dimensions in Chronic Obstructive Pulmonary Disease

The distal airways: are they important in asthma?

Differential Expression of Tissue Repair Genes in the Pathogenesis of Chronic Obstructive Pulmonary Disease

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