Evidence map›Paper›PMID 26637560›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Blunted flow-mediated responses and diminished nitric oxide synthase expression in lymphatic thoracic ducts of a rat model of metabolic syndrome.

Scott D Zawieja, Olga Gasheva, David C Zawieja, Mariappan Muthuchamy

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Pacemaking in the lymphatic system.The Journal of physiology · 2026
    Review
  3. Article
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  5. Article
  6. Lymphatic Clearance and Pump Function.Cold Spring Harbor perspectives in medicine · 2023
    Review
  7. KAmerican journal of physiology. Cell physiology · 2022
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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

4 authors at 1 institution in 1 country.

Scott D ZawiejaDepartment of Medical Physiology, College of Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center, Texas A&M University, Temple, Texas.
Olga GashevaDepartment of Medical Physiology, College of Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center, Texas A&M University, Temple, Texas.
David C ZawiejaDepartment of Medical Physiology, College of Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center, Texas A&M University, Temple, Texas.
Mariappan MuthuchamyDepartment of Medical Physiology, College of Medicine, Cardiovascular Research Institute, Division of Lymphatic Biology, Texas A&M Health Science Center, Texas A&M University, Temple, Texas marim@tamu.edu.
Texas A&M Health Science Center · US

Funding

Role of mesenteric lymphatics and dietary endotoxin in metabolic syndromeR01DK099221 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MUTHUCHAMY, MARIAPPAN, ZAWIEJA, DAVID CARL · 2013 to 2015
$976k
NIDDK NIH HHS R01 DK099221NIDDK NIH HHS R01-DK-99221
6 · The paper itself

Abstract

Shear-dependent inhibition of lymphatic thoracic duct (TD) contractility is principally mediated by nitric oxide (NO). Endothelial dysfunction and poor NO bioavailability are hallmarks of vasculature dysfunction in states of insulin resistance and metabolic syndrome (MetSyn). We tested the hypothesis that flow-dependent regulation of lymphatic contractility is impaired under conditions of MetSyn. We utilized a 7-wk high-fructose-fed male Sprague-Dawley rat model of MetSyn and determined the stretch- and flow-dependent contractile responses in an isobaric ex vivo TD preparation. TD diameters were tracked and contractile parameters were determined in response to different transmural pressures, imposed flow, exogenous NO stimulation by S-nitro-N-acetylpenicillamine (SNAP), and inhibition of NO synthase (NOS) by l-nitro-arginine methyl ester (l-NAME) and the reactive oxygen species (ROS) scavenging molecule 4-hydroxy-tempo (tempol). Expression of endothelial NO synthase (eNOS) in TD was determined using Western blot. Approximately 25% of the normal flow-mediated inhibition of contraction frequency was lost in TDs isolated from MetSyn rats despite a comparable SNAP response. Inhibition of NOS with l-NAME abolished the differences in the shear-dependent contraction frequency regulation between control and MetSyn TDs, whereas tempol did not restore the flow responses in MetSyn TDs. We found a significant reduction in eNOS expression in MetSyn TDs suggesting that diminished NO production is partially responsible for impaired flow response. Thus our data provide the first evidence that MetSyn conditions diminish eNOS expression in TD endothelium, thereby affecting the flow-mediated changes in TD lymphatic function.

Indexed as

AnimalsAntioxidantsCyclic N-OxidesEndothelium, LymphaticEnzyme InhibitorsMaleMetabolic SyndromeMuscle ContractionMuscle RelaxationNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IIIPenicillaminePulsatile FlowRatsAntioxidantsCyclic N-OxidesEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IIINos3 protein, ratPenicillamineS-nitro-N-acetylpenicillamineSpin Labelstempollymphatic endothelial cellslymphatic vessel contractionlymph flowmetabolic syndromenitric oxide synthase

Identifiers

PMID26637560
PMCPMC4796620
OpenAlexW2198075922

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.