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

• Published in: Journal of the American College of Cardiology Vol. 35; no. 2; pp. 463 - 467
• Main Authors: Tworetzky, Wayne, Moore, Phillip, Bekker, Janine M, Bristow, James, Black, Stephen M, Fineman, Jeffrey R
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.02.2000; Elsevier Science
• Subjects: Adolescent; Adult; Biological and medical sciences; Biomarkers - blood; Blood Flow Velocity; Cardiac Catheterization; Cardiac Surgical Procedures - instrumentation; Child; Child, Preschool; Diseases of the cardiovascular system; Female; Heart Septal Defects, Atrial - blood; Heart Septal Defects, Atrial - physiopathology; Heart Septal Defects, Atrial - surgery; Humans; Male; Medical sciences; Middle Aged; Nitric Oxide - biosynthesis; Nitric Oxide - blood; Prognosis; Pulmonary Artery - physiopathology; Pulmonary Circulation - physiology; Pulmonary Wedge Pressure; Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects); NO; SD; ASD; eNOS; Qs; NOx; cGMP; Qp; Regional blood flow; Pathophysiology; Persistent fetal circulation; Instrumentation therapy; Expiration; Cardiovascular disease; Exploration; Biosynthesis; Instrumental obliteration; Congenital disease; Treatment; Heart disease; Nitric oxide; Evolution; Pulmonary circulation; Hemodynamics; Ostium secundum
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(99)00576-8

OBJECTIVE To determine the effect of pulmonary blood flow (Qp) on nitric oxide (NO) production in patients with increased Qp due to an atrial septal defect (ASD). BACKGROUND Alterations in pulmonary vascular NO production have been implicated in the development of pulmonary hypertension secondary to increased Qp. In vitro, acute changes in flow or shear stress alter NO production. However, 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 ASD undergoing device closure were studied. Before, and 30 min after ASD closure, exhaled NO and plasma nitrate concentration were measured by chemiluminescence (NOA 280, Sievers, Boulder, Colorado). RESULTS Before ASD closure, all patients had increased Qp (Qp: systemic blood flow [Qs] of 2.0 ± 0.7) and normal mean pulmonary arterial pressure (13.4 ± 3.1 mm Hg). Atrial septal defect device closure decreased Qp from 6.0 ± 2.5 to 3.6 ± 1.3 L/min/m2(p < 0.05). Mean pulmonary arterial pressure 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) decreased. CONCLUSIONS These data represent the first demonstration that acute changes in Qp alter pulmonary NO production in vivo in humans. Exhaled NO determinations may provide a noninvasive assessment of pulmonary vascular NO production in patients with congenital heart disease. Potential correlations between exhaled NO, pulmonary vascular reactivity and pulmonary hypertension warrant further study.