Chronic airway infection leads to angiogenesis in the pulmonary circulation.
Hopkins, Natalie, 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
APStracts 8:0243A, 2001.
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.
Received 31 August 2000; accepted in final form 10 April 2001
APS Manuscript Number A0887-0.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 18 June 2001