ArticleArchives of disease in childhood. Fetal and neonatal edition1997
Endothelial nitric oxide synthase in hypoxic newborn porcine pulmonary vessels.
Article in Archives of disease in childhood. Fetal and neonatal edition, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 37 citations in OpenAlex.
- Enhanced NO-dependent pulmonary vasodilation limits increased vasoconstrictor sensitivity in neonatal chronic hypoxia.American journal of physiology. Heart and circulatory physiology · 2017Article
- Antenatal hypoxia and pulmonary vascular function and remodeling.Current vascular pharmacology · 2013Review
- Endothelial colony-forming cells and mesenchymal stem cells from ECMO circuits of term infants.Journal of perinatology : official journal of the California Perinatal Association · 2010Article
- Article
- The pulmonary circulation of homozygous or heterozygous eNOS-null mice is hyperresponsive to mild hypoxia.The Journal of clinical investigation · 1999Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo determine if the failure of neonatal pulmonary arteries to dilate is due to a lack of nitric oxide synthase (NOS).
methodsA monoclonal antibody to endothelial NOS was used to demonstrate the distribution and density of NOS in the developing porcine lung after a period in hypobaric hypoxia. Newborn piglets were made hypertensive by exposure to hypobaric hypoxia (50.8 kPa) from < 5 minutes of age to 2.5 days of age, 3-6 days of age or 14-17 days of age. A semiquantitative scoring system was used to assess the distribution of endothelial NOS by light microscopy.
resultsNOS was present in the arteries in all hypoxic animals. However, hypoxia from birth caused a reduction in NOS compared with those lungs normal at birth and those normal at 3 days. Hypoxia from 3-6 days led to a high density of NOS compared with normal lungs at 6 days. Hypoxia from 14-17 days had little effect on the amount of NOS. On recovery in room air after exposure to hypoxia from birth there was a transient increase in endothelial NOS after three days of recovery, mirroring that seen at three days in normal animals.
conclusionsSuppression of NOS production in the first few days of life may contribute to pulmonary hypertension in neonates.
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Registered trials
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