HIGHLIGHTED TOPICSLung Growth and RepairCommentaryGary C. SieckGary C. SieckPublished Online:01 Dec 2004https://doi.org/10.1152/japplphysiol.01049.2004MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations Difficulties associated with premature birth have focused most studies of pulmonary development on the prenatal period. However, for long-lived species such as humans and other primates, most lung growth and some lung development occur after birth. In humans, the lung continues to grow during the first eight years of life. Significant increases in lung size occur simultaneously with the need for continued differentiation of function of the lung compartments. Two papers, entitled “Epithelial cell distribution and abundance in rhesus monkey airways during postnatal lung growth and development” by Dr. L. Van Winkle and colleagues (3) and “Smooth muscle development during postnatal growth of distal bronchioles in infant rhesus monkeys” by Dr. M.-U. Tran and colleagues (2), show that despite substantial increase in airway size during the postnatal period, the density of the epithelium and the organization of smooth muscle are tightly regulated from birth. Together, these two studies quantified the cellular components of the epithelial compartment and the smooth muscle of the interstitial compartment in rhesus monkeys 5 days, 1, 2, 3, and 6 mo of age. The rhesus monkey is an excellent model for asking questions about the impact of growth (i.e., increasing size, surface area, and volume) on cell populations in the lung. The chief finding of these two studies was that the epithelium establishes an organization and density proportional to airway size, whereas smooth muscle abundance remains constant with increasing airway size. Such relationships are maintained regardless of age. Subtle differences in the orientation of smooth muscle in the most distal bronchioles occur with age, likely due to alveolarization. Although active proliferation and differentiated function are normally inversely related, these studies show that proliferation and differentiation occur simultaneously in the maturing airway, implying that the abundance and distribution of airway components are tightly coordinated. The overall goal of these studies was to establish a basis for mechanistic studies of disease in which injury and repair occur during lung growth and development. Few studies of postnatal development of the conducting airways have been completed, yet numerous epidemiologic studies of humans and basic studies of animals have established that once the lung is injured during an active period of growth (e.g., by factors such as environmental pollutants), normal lung development and repair of acute injury are compromised despite continued lung growth. In such cases, the drive for growth overrides that for repair, likely because of disruption of the tight regulation of airway components.In the third and final featured article, entitled “Quantitative models of the rat pulmonary arterial tree morphometry applied to hypoxia-induced arterial remodeling,” Dr. R. Molthen and colleagues (1) apply volumetric micro-focal X-ray-computed tomographic imaging, a relatively new technology, and recently developed quantitative models of pulmonary tree morphology to study the longitudinal distribution of vascular remodeling in a rat model of pulmonary hypertension. The focus of this study was the structure-to-function relationship in the pulmonary circulation, with the objective of better understanding the etiology, progression, and hemodynamic impact of the vascular remodeling process. Against a permissive genetic background, stimuli such as alveolar hypoxia and exposure to certain toxins, drugs, or blood-borne metabolites can lead to progressive pulmonary vascular remodeling and, ultimately, to cor pulmonale and death. Rats exposed to 10% oxygen for 21 days exhibited morphological changes that contributed to an increase in pulmonary arterial pressure. In hypoxic rats, the total length and number of branches in the pulmonary arterial tree differed significantly from those measured in normoxic controls. These data support, and notably extend, qualitative observations of structural changes to the pulmonary vasculature in both clinical and experimental pulmonary hypertension. New imaging tools and morphology-based models such as those used in this study could provide a basis for developing new strategies for clinical diagnosis, treatment, and screening for predisposition to pulmonary vasculopathy and hypertension.REFERENCES1 Molthen RC, Karau KL, and Dawson CA. Quantitative models of the rat pulmonary arterial tree morphometry applied to hypoxia-induced arterial remodeling. J Appl Physiol 97: 2372-2384, 2004.Link | ISI | Google Scholar2 Tran MUT, Weir AJ, Fanucchi MV, Rodriguez AE, Van Winkle LS, Evans MJ, Smiley-Jewell SM, Miller LA, Schelegle ES, Gershwin LJ, Hyde DM, and Plopper CG. Smooth muscle development during postnatal growth of distal bronchioles in infant rhesus monkeys. J Appl Physiol 97: 2364-2371, 2004.Link | ISI | Google Scholar3 Van Winkle LS, Fanucchi MV, Miller LA, Baker GL, Gershwin LJ, Schelegle ES, Hyde DM, Evans MJ, and Plopper CG. Epithelial cell distribution and abundance in rhesus monkey airways during postnatal lung growth and development. J Appl Physiol 97: 2355-2363, 2004.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 97Issue 6December 2004Pages 2354-2354 Copyright & PermissionsCopyright © 2004 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.01049.2004History Published online 1 December 2004 Published in print 1 December 2004 Metrics