Evidence map›Paper›PMID 23244497›Full record

ArticleAntioxidants & redox signaling2013

Reactive oxygen species-reducing strategies improve pulmonary arterial responses to nitric oxide in piglets with chronic hypoxia-induced pulmonary hypertension.

Candice D Fike, Anna Dikalova, James C Slaughter, M R Kaplowitz, Y Zhang, Judy L Aschner

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. L-Citrulline in Neonates: From Bench to Bed Side.Children (Basel, Switzerland) · 2024
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  12. Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2016
    Review
  13. Rescue Treatment with L-Citrulline Inhibits Hypoxia-Induced Pulmonary Hypertension in Newborn Pigs.American journal of respiratory cell and molecular biology · 2015
    Article
  14. Review
  15. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Candice D FikeDepartment of Pediatrics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. candice.fike@vanderbilt.edu
Anna Dikalova
James C Slaughter
M R Kaplowitz
Y Zhang
Judy L Aschner
Vanderbilt University · US

Funding

Chronic progressive hypoxia-induced pulmonary hypertension in newbornsR01HL097566 · NHLBI · VANDERBILT UNIVERSITY · PI FIKE, CANDICE D · 2010 to 2013
$2.2M
Prostanoids and Hypoxic Neonatal Pulmonary HypertensionR01HL068572 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FIKE, CANDICE D · 2002 to 2009
$2.1M
NHLBI NIH HHS R01 HL068572NHLBI NIH HHS R01 HL68572NHLBI NIH HHS R01 HL97566
6 · The paper itself

Abstract

aimsThere are no effective treatments for chronic pulmonary hypertension in infants with cardiopulmonary disorders associated with hypoxia, such as those with chronic lung disease. These patients often have poor or inconsistent pulmonary dilator responses to inhaled nitric oxide (iNO) therapy for unknown reasons. One possible explanation for poor responsiveness to iNO is reduced NO bioavailability caused by interactions between reactive oxygen species (ROS) and NO. Our major aim was to determine if strategies to reduce ROS improve dilator responses to the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), in resistance pulmonary arteries (PRAs) from a newborn piglet model of chronic pulmonary hypertension.

resultsThe dilation to SNAP was significantly impaired in PRAs from piglets with chronic hypoxia-induced pulmonary hypertension. ROS scavengers, including cell-permeable and impermeable agents to degrade hydrogen peroxide (H(2)O(2)), improved dilation to SNAP in PRAs from chronically hypoxic piglets. Treatment with agents to inhibit nitric oxide synthase and NADPH oxidase, potential enzymatic sources of ROS, also improved dilation to SNAP in PRAs from hypoxic piglets. INNOVATION: Our studies are the first to utilize a newborn model of chronic pulmonary hypertension to evaluate the impact of a number of potential therapeutic strategies for ROS removal on responses to exogenous NO in the vessels most relevant to the regulation of pulmonary vascular resistance (PRA).

conclusionsStrategies aimed at reducing ROS merit further evaluation and consideration as therapeutic approaches to improve responses to iNO in infants with chronic pulmonary hypertension.

Indexed as

HypoxiaAnimalsCatalaseDisease Models, AnimalDose-Response Relationship, DrugHypertension, PulmonaryNADPH OxidasesNitric OxideNitric Oxide Synthase Type IIIPolyethylene GlycolsPulmonary ArteryReactive Oxygen SpeciesS-Nitroso-N-AcetylpenicillamineSuperoxide DismutaseSwineCatalasecatalase-polyethylene glycolNADPH OxidasesNitric OxideNitric Oxide Synthase Type IIIPolyethylene GlycolsReactive Oxygen SpeciesS-Nitroso-N-AcetylpenicillamineSuperoxide Dismutase

Identifiers

PMID23244497
PMCPMC3619184
OpenAlexW2141075908

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.