Pulmonary blood flow alters nitric oxide production in patients undergoingdevice closure of atrial septal defects

OBJECTIVE To determine the effect of pulmonary blood flow (Qp) on nitric ox ide (NO) production in patients with increased Qp due to an atrial septal d efect (ASD). BACKGROUND Alterations in pulmonary vascular NO production have been implic ated in the development of pulmonary hypertension secondary to increased Qp . In vitro, acute changes in flow or shear stress alter NO production. Howe ver, the effect of Qp on lung NO production in vivo is unclear. METHODS Nineteen patients (2.4-61 years of age, median 17) with secundum AS D undergoing device closure were studied. Before, and 30 min after ASD clos ure, exhaled NO and plasma nitrate concentration were measured by chemilumi nescence (NOA 280, Sievers, Boulder, Colorado). RESULTS Before ASD closure, all patients had increased Qp (Qp: systemic blo od flow [Qs] of 2.0 +/- 0.7) and normal mean pulmonary arterial pressure (1 3.4 +/- 3.1 mm Hg). Atrial septal defect device closure decreased Qp from 6 .0 +/- 2.5 to 3.6 +/- 1.3 L/min/m(2) (p < 0.05). Mean pulmonary arterial pr essure was unchanged. Associated with the decrease in Qp, both exhaled NO ( -22.1%, p < 0.05) and plasma nitrate concentrations (-17.9%, p < 0.05) decr eased. CONCLUSIONS These data represent the first demonstration.that acute changes in Qp alter pulmonary NO production in vivo in humans. Exhaled NO determin ations may provide a noninvasive assessment of pulmonary vascular NO produc tion in patients with congenital heart disease. Potential correlations betw een exhaled NO, pulmonary vascular reactivity and pulmonary hypertension wa rrant further study. (J Am Coll Cardiol 2000;35:463-7) (C) 2000 by the Amer ican College of Cardiology.