ArticleIntensive care medicine2003
Endothelial nitric oxide synthase (NOS) is upregulated in rapid progressive pulmonary hypertension of the newborn.
Article in Intensive care medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Is Inducible Nitric Oxide Synthase (iNOS) Promising as a New Target Against Pulmonary Hypertension?Antioxidants (Basel, Switzerland) · 2025Review
- MIF inhibition enhances pulmonary angiogenesis and lung development in congenital diaphragmatic hernia.Pediatric research · 2019Article
- Nitric oxide synthases in infants and children with pulmonary hypertension and congenital heart disease.Respiratory research · 2009Article
- S-nitrosothiols signal hypoxia-mimetic vascular pathology.The Journal of clinical investigation · 2007Article
- Year in review in intensive care medicine-2003. Part 3: intensive care unit organization, scoring, quality of life, ethics, neonatal and pediatrics, and experimental.Intensive care medicine · 2004Review
- Epigenetic mechanisms of pulmonary hypertension.Pulmonary circulationArticle
- Endothelial dysfunction in pulmonary arterial hypertension: an evolving landscape (2017 Grover Conference Series).Pulmonary circulationArticle
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo provide evidence for the upregulation of endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) in the assumed imbalance in the pathophysiology of rapid progressive pulmonary hypertension of the newborn (RPPHN), which is characterized by abnormal hypertrophy of the pulmonary arterioles and arteries leading to increased pulmonary vascular resistance. Furthermore, to determine the cellular source and topographic distribution of eNOS and iNOS. MATERIAL AND
methodsLung biopsies were taken from two term neonates with clinical and echocardiographic evidence of RPPH and of three controls. Biopsies were obtained at an early stage of the disease as well as at post mortem and examined immunohistochemically for the presence of eNOS, iNOS and nitrotyrosine.
resultsThe endothelial cells of pulmonary arterioles stained significantly for eNOS protein in RPPHN patients. This was not the case in the control infants. There were no differences for nitrotyrosine or iNOS between RPPHN patients and controls.
conclusionRapid progressive pulmonary hypertension of the newborn leads to compensatory induction of eNOS synthesis specifically in endothelial cells of the pulmonary arterioles. This mechanism of compensation can lead to delayed presentation of RPPHN during the late neonatal period. Exogenous inhaled nitric oxide therapy does not lead to suppression of the endogenous synthesis of nitric oxide.
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