PULMONARY VEINS AND BRONCHIAL VESSELS UNDERGO REMODELING IN SUSTAINEDPULMONARY-HYPERTENSION INDUCED BY CONTINUOUS AIR EMBOLIZATION INTO SHEEP

Citation
Je. Johnson et al., PULMONARY VEINS AND BRONCHIAL VESSELS UNDERGO REMODELING IN SUSTAINEDPULMONARY-HYPERTENSION INDUCED BY CONTINUOUS AIR EMBOLIZATION INTO SHEEP, Experimental lung research, 23(5), 1997, pp. 459-473
Citations number
34
Categorie Soggetti
Respiratory System
Journal title
ISSN journal
01902148
Volume
23
Issue
5
Year of publication
1997
Pages
459 - 473
Database
ISI
SICI code
0190-2148(1997)23:5<459:PVABVU>2.0.ZU;2-E
Abstract
While it is well known that chronic pulmonary hypertension is accompan ied by characteristic structural changes in the pulmonary arteries, it is becoming increasingly apparent that the remodeling process also in volves the venous side of the circulation. The present paper utilizes a sheep model of sustained pulmonary hypertension induced by continuou s air embolization (CAE) into the pulmonary arterial circulation to ex amine the structure of the pulmonary veins and bronchial vasculature. Morphometric techniques were applied to the pulmonary veins and bronch ial vessels following distension of the venous circulation with a bari um-sulfate gelatin mixture,. this route of filling also resulted in di stension of the bronchial vessels. Four and 12 days of CAE resulted in a significant increase in the proportion of muscular pulmonary veins (e.g., percent muscular veins <75 mu m following 12 days CAE = 17.7 +/ - 6.9; controls = 0), an approximate doubling in percent venous medial thickness, and a 50% reduction in number of barium-filled peripheral vessels. Examination of the bronchial circulation revealed a striking increase in volume due both to a 50% increase in vessel diameter and a threefold increase in number of small vessels (p<.05). The authors co nclude that CAE-induced chronic pulmonary hypertension is associated w ith remodeling of both the pulmonary veins and bronchial circulation a s well as the pulmonary arteries. The mechanisms for these structural alterations are not certain, but may include local release of vasoacti ve and inflammatory mediators and an increase in bronchopulmonary anas tomoses.