Chronic airway infection leads to angiogenesis in the pulmonary circulation

In both pulmonary and systemic hypertension, the walls of the arteriolar ve ssels are thickened and the lumen size is reduced, leading to increased tot al vascular resistance. It has been reported previously that chronic airway infection and inflammation lead to increased wall thickness in the pulmona ry 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 ane sthetized and inoculated intratracheally with Pseudomonas aeruginosa (n = 1 0) incorporated into agar beads to induce chronic airway infection. Control groups included rats inoculated with sterile agar beads (n = 8) and rats t hat were not inoculated (n = 6). Chronic infection caused vascular wall thi ckening without reduction in mean lumen radius. Furthermore, chronic infect ion led to increased total length of intra-acinar vessels and increased num bers of branch points, demonstrating that angiogenesis had occurred. Preser vation of lumen size and formation of new parallel pathways in the vasculat ure of chronically infected lungs account for the maintenance of normal PVR despite vessel wall remodeling.