Evidence map›Paper›PMID 12584225›Full record

ArticleGut2003

Enhanced vasodilatation to endothelin antagonism in patients with compensated cirrhosis and the role of nitric oxide.

A Helmy, D E Newby, R Jalan, P C Hayes, D J Webb

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Endothelin-A-mediated vasoconstriction during exercise with advancing age.The journals of gerontology. Series A, Biological sciences and medical sciences · 2015
    Article
  6. Hepatosplanchnic circulation in cirrhosis and sepsis.World journal of gastroenterology · 2015
    Review
  7. Article
  8. Article
  9. Endothelin and hepatic wound healing.Pharmacological research · 2011
    Review
  10. Article
  11. Article
  12. Review
  13. Cardiopulmonary complications in chronic liver disease.World journal of gastroenterology · 2006
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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

5 authors at 2 institutions in 1 country.

A HelmyLiver Unit, Department of Medicine, Royal Infirmary of Edinburgh, and Clinical Pharmacology Unit and Research Centre, Department of Medical Sciences, University of Edinburgh, Western General Hospital, Edinburgh, UK.
D E Newby
R Jalan
P C Hayes
D J Webb
Edinburgh Royal Infirmary · GBWestern General Hospital · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

BACKGROUND AND

aimsPatients with advanced cirrhosis have systemic vasodilatation and increased nitric oxide (NO) production despite activated vasopressor systems, including the endothelin system. The aims of this study were to assess the contribution of endogenous endothelin 1 (ET-1) and NO to the maintenance of basal forearm vascular tone in patients with preascitic cirrhosis (n=7) and in age and sex matched healthy controls (n=7).

methodsUsing venous occlusion plethysmography, forearm blood flow (FBF) responses to subsystemic locally active intra-arterial infusion of BQ-123 (a selective endothelin type A receptor (ET(A)) receptor antagonist; 10 nmol/min) were measured before and during application of an "NO clamp": a balanced co-infusion of L-N(G)-monomethyl-arginine (a selective NO synthase inhibitor) and sodium nitroprusside (an exogenous NO donor) to block endogenous NO production and restore NO mediated basal FBF, respectively.

resultsL-NMMA infusion produced a reduction in FBF (p<0.001) which was similar in both groups. Before applying the "NO clamp", BQ-123 caused an increase in FBF in both groups (p<0.001) that was greater in patients with cirrhosis (p<0.01). During the "NO clamp", BQ-123 induced vasodilatation was abolished in controls and attenuated in patients (p<0.001) but remained significantly greater in patients with cirrhosis (p<0.01).

conclusionsThese findings indicate a greater ET(A) mediated contribution of endogenous ET-1 to the maintenance of basal forearm vascular tone in patients with preascitic cirrhosis. In addition, enhanced vasodilatation to ET(A) receptor antagonism in cirrhosis cannot be entirely attributed to NO release but is likely to be related to reversal of direct ET-1 mediated tone.

Indexed as

VasodilationAdultCase-Control StudiesEndothelin-1Endothelin Receptor AntagonistsEnzyme InhibitorsFemaleForearmHemodynamicsHumansLiver CirrhosisMaleMiddle AgedNitric OxideNitric Oxide Synthaseomega-N-Methylargininecyclo(Trp-Asp-Pro-Val-Leu)Endothelin-1Endothelin Receptor AntagonistsEnzyme InhibitorsNitric OxideNitric Oxide Synthaseomega-N-MethylargininePeptides, Cyclic

Identifiers

PMID12584225
PMCPMC1773556
OpenAlexW2007641683

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.