Airway vascular changes in lung allograft recipients

Citation
L. Zheng et al., Airway vascular changes in lung allograft recipients, J HEART LUN, 18(3), 1999, pp. 231-238
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HEART AND LUNG TRANSPLANTATION
ISSN journal
10532498 → ACNP
Volume
18
Issue
3
Year of publication
1999
Pages
231 - 238
Database
ISI
SICI code
1053-2498(199903)18:3<231:AVCILA>2.0.ZU;2-J
Abstract
Background: In asthma there has been increasing interest in the contributio n of airway microvasculature to airway wall thickness and lumenal narrowing . Post-lung transplant, the survival of the donor airway is generally depen dent on mixed-venous blood flow from pulmonary artery collaterals associate d with the discontinuation of the bronchial circulation. This may lead to a n altered vasculature of the airways post transplant, which may contribute to airflow limitation. Methods: Endobronchial biopsies were taken from the lower lobe sub-carinae in 22 lung transplant recipients (LTR), 8 with Bronchiolitis Obliterans Syn drome (BOS), 14 without, and 14 controls. Seven mu m frozen sections were s tained for type IV collagen with a monoclonal antibody, using an indirect i mmunoperoxidase method. Bronchial vessels were identified by typical staini ng of type IV collagen in the true basement membrane supporting the endothe lium. The number of vessels per mm(2) of submucosa to a depth of 150 mu m b elow. the basement membrane, the percent vascularity and average vessel siz e were quantified using a computerised image analyser. Results: Compared to the controls, a higher percent vascularity was found i n LTR both with and without BOS (p < 0.05). In the BOS group, the percent b est FEV1.0 decreased exponentially, in association with increased airway ve ssel size (r(2) = 0.67, p = 0.01). Conclusions: These findings suggest that increased airway vascularity is a feature of the allograft airways post transplant. This may be a result of t he relative hypoxia and hypercarbia in the blood supplying the airways from the pulmonary artery collaterals or of the chronic inflammatory process in the airways. These changes in vascularity could contribute to airflow limi tation in BOS.