Evidence map›Paper›PMID 28733445›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2017

Enhanced NO-dependent pulmonary vasodilation limits increased vasoconstrictor sensitivity in neonatal chronic hypoxia.

Joshua R Sheak, Laura Weise-Cross, Ray J deKay, Benjimen R Walker, Nikki L Jernigan, Thomas C Resta

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. The role of RNA mRespiratory research · 2021
    Article
  3. Article
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.

Joshua R SheakVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.ORCID http://orcid.org/0000-0002-8002-4365
Laura Weise-CrossVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Ray J deKayVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Benjimen R WalkerVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Nikki L JerniganVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico.
Thomas C RestaVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico tresta@salud.unm.edu.
University of New Mexico · US

Funding

FAIR Data Competency and Machine Learning Readiness for Biomedical ScientistsK12GM088021 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI REBECCA S. HARTLEY, Diane Lidke · 2009 to 2026
$16.4M
MINORITY INSTITUTIONAL RESEARCH TRAINING PROGRAM (T32)T32HL007736 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 1993 to 2025
$6.5M
Pulmonary Vasoreactivity Following Chronic HypoxiaR01HL088192 · NHLBI · UNIVERSITY OF NEW MEXICO · PI RESTA, THOMAS C · 2008 to 2012
$1.9M
Vascular Smooth Muscle Signaling in Intermittent Hypoxia-Induced Pulmonary HypertensionR01HL132883 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI RESTA, THOMAS C · 2016 to 2019
$1.5M
Role of PKCbeta and oxidant signaling in neonatal pulmonary hypertensionF31HL131334 · NHLBI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI SHEAK, JOSHUA ROGER · 2016 to 2017
$47k
NHLBI NIH HHS F31 HL131334NHLBI NIH HHS R01 HL088192NHLBI NIH HHS R01 HL132883NHLBI NIH HHS T32 HL007736NIGMS NIH HHS K12 GM088021
6 · The paper itself

Abstract

Augmented vasoconstrictor reactivity is thought to play an important role in the development of chronic hypoxia (CH)-induced neonatal pulmonary hypertension. However, whether this response to CH results from pulmonary endothelial dysfunction and reduced nitric oxide (NO)-mediated vasodilation is not well understood. We hypothesized that neonatal CH enhances basal tone and pulmonary vasoconstrictor sensitivity by limiting NO-dependent pulmonary vasodilation. To test this hypothesis, we assessed the effects of the NO synthase (NOS) inhibitor

Indexed as

Nitric OxidePulmonary CirculationVasodilation15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic AcidAnimalsAnimals, NewbornChronic DiseaseEnzyme InhibitorsFree Radical ScavengersHypoxiaLungNitric Oxide SynthaseNitroarginineRatsRats, Sprague-DawleyTyrosine15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid3-nitrotyrosineEnzyme InhibitorsFree Radical ScavengersNitric OxideNitric Oxide SynthaseNitroarginineTyrosineVasoconstrictor Agentsendothelial nitric oxide synthase phosphorylationin situ perfused lungneonatal pulmonary hypertensionnitric oxide

Identifiers

PMID28733445
PMCPMC5668609
OpenAlexW2736629136

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.