© 2003 American Thoracic Society
Tethering Tracheobronchial Airways within the LungsCenter for Comparative Respiratory Biology and Medicine School of Veterinary Medicine University of California Davis, California The report by Elliot and colleagues (1) in this issue of AJRCCM (pp. 45–49) proposes a structural mechanism for the elevated airway responsiveness and collapsibility associated with in utero and/or postnatal cigarette smoke exposure in children. To study this relationship, Elliot and colleagues (1) examined the lungs of children who had died from sudden infant death syndrome. The alteration they detected was a decrease in the attachment of interalveolar septa to the airway wall, which they interpreted as a decrease in the anchoring for conducting airways that would influence airway function. The underlying assumption of their study is that the principal anchoring mechanism for opposing the radial collapse that produces airway narrowing is the attachment to the airways of adjacent alveolar tissue to form a close mechanical coupling between the much larger alveolar area and the conducting airways (see Figure E1 in the online supplement). The need for some form of external support structure is reasonable because the components of conducting airway walls (epithelium, connective tissue, and smooth muscle), with the exception of small cartilage plates in more proximal airways, offer little intrinsic support for maintaining either luminal patency or the three-dimensional geometry necessary for efficient aerodynamics. From an anatomic perspective, however, the interalveolar septa attached to airway walls are not the only potential structures capable of providing support to conducting airways (2). The pulmonary arteries form a tubular system, which, although intrinsically as flaccid as the airways, is in living systems highly turgid secondary to the presence of luminal fluids under pressure. As the data of Elliot and colleagues elucidate (see Table 2 in Reference 1), the pulmonary artery is closely attached by its tunica adventitia to the adventitia of the airway (see Figure E1 in the online supplement). This attachment occupies approximately one third of the circumference of the wall of the airways; it appears to have a larger total surface area for attachment than the area accumulated by the sum of all the septal attachments in the same region. For more proximal airways closer to the hilum, the pulmonary veins also share connective tissue elements with airway walls, giving those airways three potential anchors (see Figure E1 in the online supplement). Over the extent of most of the intrapulmonary bronchial tree, at least two sources of tethering for the airways could contribute to radial patency: the pulmonary artery and the interalveolar septa. The critical nature of the alveolar source of anchoring is highlighted by studies such as that of Bellofiore and coworkers (3). These authors demonstrated that a reduction in the number of interalveolar septa, achieved by experimental elastase treatment, did not produce marked elevation in airway resistance in response to methacholine except at end-expiratory volumes. In addition to the radial force exerted on the airway wall by interalveolar septa and blood vessels, the force applied longitudinally to airways, secondary to the attachment of interalveolar septa to the distal ends of bronchioles, is potentially important. As alveoli expand during inspiration, the septa forming alveolar ducts are likely to apply a force to the airways that will stretch them longitudinally. In so doing, the angle of branching is also altered (see Figure E1 in the online supplement). This would apply stress to the airway in a number of planes. In combination with a rigid anchor provided by the turgid arteries, these forces may play an equally important role in maintaining patency. In fact, the most significant change in shape of the airway wall during inspiration and expiration may not be change in radial diameter but change in length. The impact of alveolar attachment forces on regulation of airway diameter does not appear to be as significant as that of airway smooth muscle tone, at least at high distending pressures associated with deep inspiration (4). Moreover, changes in airway diameter during expiration could not be detected by high-resolution computed tomography (4). A considerable proportion of the smooth muscle bundles in airway walls, especially in more distal bronchioles, are oriented in a helical pattern, positioning them to produce airway shortening on contraction while serving as part of a functional unit with pulmonary stretch receptors to sense lung volume (5, 6). Increases in activity of pulmonary stretch receptors associated with lung inflation cause a reflex reduction in airway tone (6). The latter observation suggests that increasing airway tone during expiration plays a role in retracting the airways toward their branch points and maintaining their integrity. The smooth muscle fibers occupying branch points also are arranged parallel to the long axis of the parent airway, thus positioning them for the same two functions (5, 6). Taken together, there are a variety of sources of tethering for conducting airways within lung parenchyma that can apply stretching forces to the wall: interalveolar septa attached to the adventitial surface of the wall, turgid pulmonary arteries occupying a significant portion of the wall (especially arteries attached to the full length of the airway tree), and interalveolar septa connected around the entire end of each terminal bronchiole. Each form of tethering is positioned to contribute uniquely to the aerodynamic conformation of the airway tree as the lung parenchyma changes volume during respiration. The major challenge emphasized by the study of Elliot and colleagues (1) lies in defining these contributions and their impact in respiratory diseases (such as asthma and emphysema) where airway luminal reduction or collapse is a major clinical manifestation. FOOTNOTES This editorial has an online supplement, which is accessible from this issue's table of contents online at www.atsjournals.org REFERENCES
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