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Surgically induced unilateral pulmonary hypertension: time-related analysis of a new experimental model

Corno, Antonio F. ; Tozzi, Piergiorgio ; Genton, Claude Y. ; von Segesser, Ludwig K.

In: European Journal of Cardio-Thoracic Surgery, 2003, vol. 23, no. 4, p. 513-517

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    Titel
    • Surgically induced unilateral pulmonary hypertension: time-related analysis of a new experimental model
    Autor
    • Corno, Antonio F.. Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland
    • Tozzi, Piergiorgio. Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland
    • Genton, Claude Y.. Department of Pathology, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland
    • von Segesser, Ludwig K.. Department of Cardiovascular Surgery, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • European Journal of Cardio-Thoracic Surgery, 2003, vol. 23, no. 4, p. 513-517. Elsevier Science B.V.
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:302392
    Summary
    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 FiO2=1.0 ventilation; in the right pulmonary artery there was a mild elevation of the pressures, but still responsive (P<0.05) to FiO2=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