BACKGROUND: Nitric oxide (NO) is known to modulate myocardial contraction and coronary tone, and its inhalation reduces pulmonary vascular resistance in patients with pulmonary hypertension. OBJECTIVES: To evaluate the pathophysiological role of NO in patients with a ventricular septal defect (VSD). PATIENTS: Twenty-nine children with VSD, nine of whom had undergone VSD closure surgery, and 14 patients with Kawasaki disease. The mean age of the VSD patients was 3.1 years (range, 2 months to 9 years). METHODS: Using high performance liquid chromatography, nitrate (a more stable NO oxidation product) was measured in plasma specimens of the patients undergoing cardiac catheterisation. RESULTS: Nitrate concentrations in the pulmonary artery bore a significant relation to mean pulmonary artery pressure, pulmonary to systemic systolic pressure ratio, and pulmonary to systemic flow ratio. CONCLUSIONS: The concentration of nitrate was in proportion to the increment in intravascular or cardiac pressure, indicating that endogenous NO is upregulated as a compensatory homeostatic attempt to reduce pulmonary pressure and blood flow.
BACKGROUND:Nitric oxide (NO) is known to modulate myocardial contraction and coronary tone, and its inhalation reduces pulmonary vascular resistance in patients with pulmonary hypertension. OBJECTIVES: To evaluate the pathophysiological role of NO in patients with a ventricular septal defect (VSD). PATIENTS: Twenty-nine children with VSD, nine of whom had undergone VSD closure surgery, and 14 patients with Kawasaki disease. The mean age of the VSDpatients was 3.1 years (range, 2 months to 9 years). METHODS: Using high performance liquid chromatography, nitrate (a more stable NO oxidation product) was measured in plasma specimens of the patients undergoing cardiac catheterisation. RESULTS:Nitrate concentrations in the pulmonary artery bore a significant relation to mean pulmonary artery pressure, pulmonary to systemic systolic pressure ratio, and pulmonary to systemic flow ratio. CONCLUSIONS: The concentration of nitrate was in proportion to the increment in intravascular or cardiac pressure, indicating that endogenous NO is upregulated as a compensatory homeostatic attempt to reduce pulmonary pressure and blood flow.
Authors: K Nishida; D G Harrison; J P Navas; A A Fisher; S P Dockery; M Uematsu; R M Nerem; R W Alexander; T J Murphy Journal: J Clin Invest Date: 1992-11 Impact factor: 14.808
Authors: A Wennmalm; G Benthin; A Edlund; L Jungersten; N Kieler-Jensen; S Lundin; U N Westfelt; A S Petersson; F Waagstein Journal: Circ Res Date: 1993-12 Impact factor: 17.367