Evidence map›Paper›PMID 25534145›Full record

ArticleRespiratory physiology & neurobiology2015

Endothelial nitric oxide synthase uncoupling: a novel pathway in OSA induced vascular endothelial dysfunction.

Saradhadevi Varadharaj, Kyle Porter, Adam Pleister, Jacob Wannemacher, Angela Sow, David Jarjoura, Jay L Zweier, Rami N Khayat

Open access · greenAbstract read
In one paragraph

Article in Respiratory physiology & neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Saradhadevi VaradharajThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States; Division of Pulmonary Critical Care and Sleep, The Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, the Ohio State University, Columbus, OH, United States.
Kyle PorterThe Center for Biostatistics, the Ohio State University, Columbus, OH, United States.
Adam PleisterThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States.
Jacob WannemacherThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States.
Angela SowThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States.
David JarjouraThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States.
Jay L ZweierThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States; Division of Pulmonary Critical Care and Sleep, The Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, the Ohio State University, Columbus, OH, United States.
Rami N KhayatThe Sleep Heart Program, the Ohio State University, Columbus, OH, United States; Division of Pulmonary Critical Care and Sleep, The Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, the Ohio State University, Columbus, OH, United States. Electronic address: rami.khayat@osumc.edu.
The Ohio State University · US

Funding

Integration of High Field MRI and EPRI For Functional ImagingR01EB016096 · NIBIB · OHIO STATE UNIVERSITY · PI ZWEIER, JAY LOUIS · 2013 to 2016
$2.3M
The Microcirculation in OSAR21HL106283 · NHLBI · OHIO STATE UNIVERSITY · PI KHAYAT, RAMI N · 2011 to 2012
$419k
NHLBI NIH HHS R21 HL106283NIBIB NIH HHS R01 EB016096
6 · The paper itself

Abstract

The mechanism of vascular endothelial dysfunction (VED) and cardiovascular disease in obstructive sleep apnea (OSA) is unknown. We performed a comprehensive evaluation of endothelial nitric oxide synthase (eNOS) function directly in the microcirculatory endothelial tissue of OSA patients who have very low cardiovascular risk status. Nineteen OSA patients underwent gluteal biopsies before, and after effective treatment of OSA. We measured superoxide (O2(•-)) and nitric oxide (NO) in the microcirculatory endothelium using confocal microscopy. We evaluated the effect of the NOS inhibitor l-Nitroarginine-Methyl-Ester (l-NAME) and the NOS cofactor tetrahydrobiopterin (BH4) on endothelial O2(•-) and NO in patient endothelial tissue before and after treatment. We found that eNOS is dysfunctional in OSA patients pre-treatment, and is a source of endothelial O2(•-) overproduction. eNOS dysfunction was reversible with the addition of BH4. These findings provide a new mechanism of endothelial dysfunction in OSA patients and a potentially targetable pathway for treatment of cardiovascular risk in OSA.

Indexed as

AdultBiopterinsCardiovascular DiseasesContinuous Positive Airway PressureEndotheliumEnzyme InhibitorsFemaleHumansMaleMiddle AgedNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIISleep Apnea, ObstructiveBiopterinsEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIsapropterinEndothelial dysfunctionHypertensionNitric oxideObstructive sleep apnea

Identifiers

PMID25534145
PMCPMC4297730
OpenAlexW2018479685

What OpenQuestion holds

Textmetadata
LicenceTDM
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.