Evidence map›Paper›PMID 24819742›Full record

ArticleThe Journal of surgical research2014

Evidence against a systemic arterial defect in patients with inflammatory bowel disease.

Luke A Neill, Christine M Saundry, Neil H Hyman, George C Wellman

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

Article in The Journal of surgical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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.

Luke A NeillDepartment of Surgery, University of Vermont College of Medicine, Burlington, Vermont.
Christine M SaundryDepartment of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont.
Neil H HymanDepartment of Surgery, College of Medicine, University of Vermont, Burlington, Vermont. Electronic address: neil.hyman@vtmednet.org.
George C WellmanDepartment of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont; Department of Surgery, College of Medicine, University of Vermont, Burlington, Vermont.
University of Vermont · US

Funding

Impact of SAH on Parenchymal Arterioles and Neurovascular CouplingP01HL095488 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BONEV, ADRIAN · 2010 to 2014
$11.4M
Center for Neuroscience ExcellenceP30GM103498 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI PARSONS, RODNEY L · 2012 to 2015
$4.3M
NHLBI NIH HHS P01 HL095488NIGMS NIH HHS P30 GM103498
6 · The paper itself

Abstract

backgroundDespite increasing interest in local microvascular alterations associated with inflammatory bowel disease (IBD), the potential contribution of a primary systemic vascular defect in the etiology of IBD is unknown. We compared reactivity of large diameter mesenteric arteries from segments affected by Crohn disease (CD) or ulcerative colitis (UC) to an uninvolved vascular bed in both IBD and control patients.

methodsMesenteric and omental arteries were obtained from UC, CD, and non-IBD patients. Isometric arterial contractions were recorded in response to extracellular potassium (K(+)) and cumulative additions of norepinephrine (NE). In addition, relaxation in response to pinacidil, an activator of adenosine triphosphate-sensitive K(+) channels was examined.

resultsContraction to K(+) and sensitivity to NE were not significantly different in arteries from CD, UC, and controls. Relaxation to pinacidil was also similar between groups.

conclusionsPotassium-induced contractions and sensitivity to NE and pinacidil were not significantly different in large diameter mesenteric and omental arteries obtained from IBD patients. Furthermore, there was no significant difference in the sensitivity to K(+), NE, and pinacidil between mesenteric and omental arteries of CD and UC patients and those from non-IBD patients. Our results suggest an underlying vascular defect systemic to CD or UC patients is unlikely to contribute to the etiology of IBD.

Indexed as

Calcium ChannelsHumansInflammatory Bowel DiseasesMesenteric ArteriesNorepinephrinePinacidilPotassiumVasoconstrictionVasodilationCalcium ChannelsNorepinephrinePinacidilPotassiumCrohn diseaseInflammatory bowel diseaseMesenteric arteryNorepinephrinePinacidilPotassiumUlcerative colitis

Identifiers

PMID24819742
PMCPMC4160373
OpenAlexW2161185019

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.