Evidence map›Paper›PMID 31247004›Full record

ArticlePloS one2019

Sepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis model.

Soeren Erik Pischke, Siv Hestenes, Harald Thidemann Johansen, Hilde Fure, Jan Frederik Bugge, Andreas Espinoza, Helge Skulstad, Thor Edvardsen, Erik Fosse, Tom Eirik Mollnes and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  13. Right Ventricular Dysfunction Score in the Prognostic Evaluation of Patients with Sepsis and Septic Shock.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine
    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

12 authors at 3 institutions in 1 country.

Soeren Erik PischkeDepartment of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.ORCID 0000-0003-2543-3251
Siv HestenesIntervention Centre, Oslo University Hospital, Oslo, Norway.
Harald Thidemann JohansenDepartment of Pharmaceutical Biosciences, School of Pharmacy, University of Oslo, Oslo, Norway.
Hilde FureResearch Laboratory, Nordland Hospital, Bodø, and Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway.
Jan Frederik BuggeDepartment of Anaesthesiology, Division of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway.
Andreas EspinozaDepartment of Anaesthesiology, Division of Emergencies and Critical Care, Oslo University Hospital, Oslo, Norway.
Helge SkulstadFaculty of Medicine, University of Oslo, Oslo, Norway.
Thor EdvardsenFaculty of Medicine, University of Oslo, Oslo, Norway.
Erik FosseFaculty of Medicine, University of Oslo, Oslo, Norway.
Tom Eirik MollnesDepartment of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.
Per Steinar HalvorsenFaculty of Medicine, University of Oslo, Oslo, Norway.
Erik Waage NielsenDepartment of Immunology, University of Oslo and Oslo University Hospital, Oslo, Norway.ORCID 0000-0002-8358-3226
Oslo University Hospital · NONordland Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRight ventricular (RV) myocardial dysfunction is a common feature in septic shock. It can worsen outcome, but the etiology is poorly understood. Pulmonary artery hypertension (PAH) plays a part in the pathogenesis of the right heart dysfunction in sepsis but its importance is unknown. In pigs, PAH in sepsis is substantial and the translational value of porcine sepsis models therefore questioned. We hypothesized that porcine sepsis causes a myocardial inflammatory response which leads to myocardial dysfunction independent of PAH. MATERIALS AND

methodsSepsis was induced by Escherichia coli-infusion in 10 pigs resulting in PAH and increased right ventricular pressure (RVP). The same degree of RVP was achieved by external pulmonary artery banding (PAB) in a consecutive series of 6 animals.

resultsSepsis, but not PAB, led to increase in endothelial damage marker PAI-1 and cytokines TNF and IL-6 (all p<0.05) in plasma. In myocardium, TNF and IL-6 were significantly elevated in sepsis, TNF in both ventricles and IL-6 mostly in RV, while IL-1β, IL-18 and C5a were significantly higher in RV compared to LV after PAB (all p<0.05). Myocardial mRNA levels of IL-1β, IL-6, IL-18, IP-10, E-selectin and PAI-1 were significantly elevated in RV and LV during sepsis compared to PAB, while Caspase-1 was decreased in septic compared to PAB animals (all p<0.05). Cathepsin L activity was increased in RV by PAB, while sepsis inhibited this response. Escherichia coli-induced sepsis caused myocardial inflammation independent of PAH.

conclusionProminent PAH should therefore not exclude porcine sepsis models to further our understanding of human sepsis.

Indexed as

AnimalsCytokinesDisease Models, AnimalFemaleHypertension, PulmonaryHypertrophy, Right VentricularMaleMyocarditisMyocardiumPlasminogen Activator Inhibitor 1RNA, MessengerSepsisSus scrofaVentricular Dysfunction, RightCytokinesPlasminogen Activator Inhibitor 1RNA, Messenger

Identifiers

PMID31247004
PMCPMC6597071
OpenAlexW2953995325

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Registered trials

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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.