Abstract 2074
Pulmonary: General Lung Biology Poster Symposium, Sunday, 5/2
Introduction: Children with congenital heart disease and increased pulmonary blood flow are known to have decreased lung compliance and recurrent pulmonary infections. The etiology of these pulmonary aberrations remains unknown. Recent studies show that increased pulmonary blood flow and/or vascular pressure may influence the alveolar fluid in patients with congenital heart disease. The alveolar fluid is composed of surfactant components which are responsible for lowering the surface tension at the air liquid interface, preventing alveolar collapse at low lung volumes. Deficiencies of surfactant are known to result in decreased lung compliance and respiratory failure. In addition, recent data demonstrate that surfactant plays an important role in pulmonary host defense. Recent in vivo and in vitro data suggest that mechanical forces alter the expression of surfactant in the lung. Increased pulmonary blood flow secondary to congenital heart disease produces increases in vascular shear stress. Alterations in shear stress regulate endothelial function, but their effects on pulmonary alveolar epithelial function have not been investigated. We have recently established a model of pulmonary hypertension secondary to increased pulmonary blood flow in the lamb following in utero placement of an aortopulmonary vascular graft. The purpose of the present study was to utilize our animal model to determine the effect of increased pulmonary blood flow on the expression of surfactant protein A (SP-A).
