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Published ahead of print on October 6, 2005, doi:10.1164/rccm.200506-927OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 2, January 2006, 204-211

A more recent version of this article appeared on January 15, 2006
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Submitted on June 15, 2005
Accepted on October 6, 2005

Growth of the Pulmonary Microvasculature in Ventilated Preterm Infants

Monique E De Paepe1*, Quanfu Mao1, Jessica Powell2, Sam E Rubin1, Philip DeKoninck2, Naomi Appel2, Meredith Dixon1, and Fusun Gundogan1

1 Department of Pathology, Women and Infants Hospital, Providence, RI, USA; Department of Pathology, Brown Medical School, Providence, RI, USA, 2 Department of Pathology, Women and Infants Hospital, Providence, RI, USA

* To whom correspondence should be addressed. E-mail: mdepaepe{at}wihri.org.

Rationale. Density-based morphometric studies have demonstrated decreased capillary density in infants with bronchopulmonary dysplasia (BPD) and in BPD-like animal models, leading to the prevailing view that microvascular development is disrupted in BPD. Objective. To perform a comprehensive analysis of the early and late effects of ventilation on pulmonary microvascular growth in preterm infants. Methods. Postmortem lung samples were collected from ventilated preterm infants who died between 23-29 weeks ("short-term ventilated") or between 36-39 weeks ("long-term ventilated") corrected postmenstrual age. Results were compared with age-matched infants or stillborns ("early" and "late" controls). Microvascular growth was studied by anti-platelet endothelial cell adhesion molecule (PECAM)-1 immunohistochemistry, quantitative stereology, analysis of endothelial cell proliferation, and Western blot analysis of pulmonary PECAM-1 protein levels. Measurements. Capillary density (AA[end/ae]); volume of air-exchanging parenchyma (V[ae]); volume of microvascular endothelial cells (V[end]); Ki67 labeling index of endothelial cells; PECAM-1/actin protein levels. Main Results. Lungs of long-term ventilated infants showed a significant more than two-fold increase of V(ae) and a 60% increase of total pulmonary microvascular endothelial volume (V[end]) compared with late controls, associated with 60% higher pulmonary PECAM-1 protein levels. The marked expansion of the pulmonary microvasculature in ventilated lungs was, at least partly, attributable to brisk endothelial cell proliferation. The microvasculature of ventilated lungs appeared immature, retaining a saccular architectural pattern. Conclusions. The pulmonary microvasculature of ventilated preterm infants displays marked angiogenesis, nearly proportionate to the growth of the air-exchanging lung parenchyma. These results challenge the paradigm of microvascular growth arrest as major pathogenic factor in BPD.
Key words: Chronic lung disease of prematurity, bronchopulmonary dysplasia, neonatal lung disease




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