Urinary nitrite and nitrate concentrations in patients with idiopathic persistent pulmonary hypertension of the newborn and effect of extracorporeal membrane oxygenation

Shaul Dollberg, Brad W. Warner, Leslie Myatt

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37 Citations (Scopus)

Abstract

Persistent pulmonary hypertension of the newborn (PPHN) often requires extracorporeal membrane oxygenation (ECMO), during which time pulmonary vascular resistance gradually declines. Nitric oxide (NO) is a recently recognized pulmonary vasodilator, but its role in PPHN is unknown. We tested the hypothesis that the concentrations of the urinary metabolites of NO, i.e. nitrite and nitrate, are reduced in patients with PPHN and increase during ECMO as the PPHN resolves. Eight newborn infants with PPHN on ECMO were studied. Daily urinary concentrations of nitrite/nitrate were measured. We found that mean urinary concentrations of nitrite/nitrate were lower in patients with PPHN than in 47 controls without pulmonary disease (p <0.005). Urinary nitrite/nitrate concentration showed an initial increase after initiation of ECMO. However, a decrease to concentrations still lower than controls occurred on the day before decannulation. We conclude that intrinsic NO production is significantly lower in patients with PPHN than in controls but increases with oxygenation. We speculate that decreased urinary NO metabolite concentrations imply a role for NO deficiency in the pathogenesis of PPHN.

Original languageEnglish (US)
Pages (from-to)31-34
Number of pages4
JournalPediatric Research
Volume37
Issue number1
StatePublished - 1995
Externally publishedYes

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Persistent Fetal Circulation Syndrome
Extracorporeal Membrane Oxygenation
Nitrites
Nitrates
Nitric Oxide
Familial Primary Pulmonary Hypertension
Vasodilator Agents
Vascular Resistance
Lung Diseases
Newborn Infant
Lung

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

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abstract = "Persistent pulmonary hypertension of the newborn (PPHN) often requires extracorporeal membrane oxygenation (ECMO), during which time pulmonary vascular resistance gradually declines. Nitric oxide (NO) is a recently recognized pulmonary vasodilator, but its role in PPHN is unknown. We tested the hypothesis that the concentrations of the urinary metabolites of NO, i.e. nitrite and nitrate, are reduced in patients with PPHN and increase during ECMO as the PPHN resolves. Eight newborn infants with PPHN on ECMO were studied. Daily urinary concentrations of nitrite/nitrate were measured. We found that mean urinary concentrations of nitrite/nitrate were lower in patients with PPHN than in 47 controls without pulmonary disease (p <0.005). Urinary nitrite/nitrate concentration showed an initial increase after initiation of ECMO. However, a decrease to concentrations still lower than controls occurred on the day before decannulation. We conclude that intrinsic NO production is significantly lower in patients with PPHN than in controls but increases with oxygenation. We speculate that decreased urinary NO metabolite concentrations imply a role for NO deficiency in the pathogenesis of PPHN.",
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AU - Dollberg, Shaul

AU - Warner, Brad W.

AU - Myatt, Leslie

PY - 1995

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N2 - Persistent pulmonary hypertension of the newborn (PPHN) often requires extracorporeal membrane oxygenation (ECMO), during which time pulmonary vascular resistance gradually declines. Nitric oxide (NO) is a recently recognized pulmonary vasodilator, but its role in PPHN is unknown. We tested the hypothesis that the concentrations of the urinary metabolites of NO, i.e. nitrite and nitrate, are reduced in patients with PPHN and increase during ECMO as the PPHN resolves. Eight newborn infants with PPHN on ECMO were studied. Daily urinary concentrations of nitrite/nitrate were measured. We found that mean urinary concentrations of nitrite/nitrate were lower in patients with PPHN than in 47 controls without pulmonary disease (p <0.005). Urinary nitrite/nitrate concentration showed an initial increase after initiation of ECMO. However, a decrease to concentrations still lower than controls occurred on the day before decannulation. We conclude that intrinsic NO production is significantly lower in patients with PPHN than in controls but increases with oxygenation. We speculate that decreased urinary NO metabolite concentrations imply a role for NO deficiency in the pathogenesis of PPHN.

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