Hemodynamic unloading leads to regression of pulmonary vascular disease in rats
Open Access
- 1 February 2001
- journal article
- Published by Elsevier in The Journal of Thoracic and Cardiovascular Surgery
- Vol. 121 (2) , 279-289
- https://doi.org/10.1067/mtc.2001.111657
Abstract
No abstract availableKeywords
This publication has 20 references indexed in Scilit:
- Complete reversal of fatal pulmonary hypertension in rats by a serine elastase inhibitorNature Medicine, 2000
- Elastase and matrix metalloproteinase inhibitors induce regression, and tenascin-C antisense prevents progression, of vascular diseaseJournal of Clinical Investigation, 2000
- Regression of Hypertrophied Rat Pulmonary Arteries in Organ Culture Is Associated With Suppression of Proteolytic Activity, Inhibition of Tenascin-C, and Smooth Muscle Cell ApoptosisCirculation Research, 1999
- Regulation of Tenascin-C, a Vascular Smooth Muscle Cell Survival Factor that Interacts with the αvβ3 Integrin to Promote Epidermal Growth Factor Receptor Phosphorylation and GrowthThe Journal of cell biology, 1997
- Tenascin-C Is Induced With Progressive Pulmonary Vascular Disease in Rats and Is Functionally Related to Increased Smooth Muscle Cell ProliferationCirculation Research, 1996
- The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.Journal of Clinical Investigation, 1996
- Extracorporeal membrane oxygenation and the treatment of critical pulmonary hypertension in congenital heart diseaseEuropean Journal of Cardio-Thoracic Surgery, 1995
- Pediatric lung transplantation for pulmonary hypertension and congenital heart diseaseThe Annals of Thoracic Surgery, 1992
- Vascular structure in lung tissue obtained at biopsy correlated with pulmonary hemodynamic findings after repair of congenital heart defects.Circulation, 1984
- Lung biopsy in congenital heart disease: a morphometric approach to pulmonary vascular disease.Circulation, 1978