Surgically induced unilateral pulmonary hypertension: time-related analysis of a new experimental model.
OBJECTIVE
Patients with irreversible pulmonary vascular obstructive disease caused by pulmonary hypertension due to congenital heart defects are considered either inoperable or only candidates to lung transplantation. This study evaluated an experimental model of surgically induced unilateral pulmonary hypertension.


METHODS
In eight pigs, 2-months-old, the left pulmonary artery was divided at the origin and end-to-side anastomosed to the descending thoracic aorta through a left thoracotomy. In this way, increased pulmonary blood flow in the right lung and systemic perfusion pressure and oxygenation in the left lung were obtained. After an interval of 6-12 weeks the animals underwent cardiac catheterization and were then sacrificed. Histological examination was done on both the lungs.


RESULTS
The mean left-to-right shunt through the left pulmonary artery diminished from 58.9+/-9.6% at the end of the procedure to 4.5+/-1.5% at the latest hemodynamic evaluation (P<0.01). Pressures and saturations remained identical in aorta and left pulmonary artery, without reduction (NS) with FiO(2)=1.0 ventilation; in the right pulmonary artery there was a mild elevation of the pressures, but still responsive (P<0.05) to FiO(2)=1.0 ventilation. Lung histology showed normal right pulmonary arteries, but irreversible vascular lesions like intimal fibrosis, medial hypertrophy, vascular occlusions, plexiform and dilatation lesions in all the left lungs.


CONCLUSIONS
The lung exposed to systemic pressure and oxygenation develops irreversible vascular lesions typical of pulmonary vascular obstructive disease. The lung exposed to increased flow shows only mild elevation of the arterial pressure, remains responsive to oxygen vasodilatation, and displays normal histology.
Corno
Antonio F
AF
Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. antonio.corno@chuv.hospvd.ch
Tozzi
Piergiorgio
P
Genton
Claude Y
CY
von Segesser
Ludwig K
LK
D000818:Animals; D006976:Hypertension, Pulmonary / Q000473:pathology / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology; D023421:Models, Animal; D011651:Pulmonary Artery / Q000473:pathology; D013552:Swine; D013997:Time Factors; D014655:Vascular Resistance