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J Appl Physiol 91: 919-928, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 2, 919-928, August 2001

Chronic airway infection leads to angiogenesis in the pulmonary circulation

Natalie Hopkins, Elaine Cadogan, Shay Giles, and Paul McLoughlin

Department of Human Anatomy and Physiology, Conway Institute of Biomolecular and Biomedical Research, University College, Earlsfort Terrace, Dublin 2, Ireland

In both pulmonary and systemic hypertension, the walls of the arteriolar vessels are thickened and the lumen size is reduced, leading to increased total vascular resistance. It has been reported previously that chronic airway infection and inflammation lead to increased wall thickness in the pulmonary vasculature, without the development of pulmonary hypertension. The aim of the present study was to examine quantitatively the remodeling of intra-acinar blood vessels in chronically infected rat lungs. Adult rats were anesthetized and inoculated intratracheally with Pseudomonas aeruginosa (n = 10) incorporated into agar beads to induce chronic airway infection. Control groups included rats inoculated with sterile agar beads (n = 8) and rats that were not inoculated (n = 6). Chronic infection caused vascular wall thickening without reduction in mean lumen radius. Furthermore, chronic infection led to increased total length of intra-acinar vessels and increased numbers of branch points, demonstrating that angiogenesis had occurred. Preservation of lumen size and formation of new parallel pathways in the vasculature of chronically infected lungs account for the maintenance of normal PVR despite vessel wall remodeling.

Pseudomonas aeruginosa; isolated-perfused lungs; stereology; pulmonary hypertension


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