Evidence map›Paper›PMID 29084268›Full record

ArticlePloS one2017

Early structural changes of the heart after experimental polytrauma and hemorrhagic shock.

Christian K Braun, Miriam Kalbitz, Rebecca Halbgebauer, Philipp Eisele, David A C Messerer, Sebastian Weckbach, Anke Schultze, Sonja Braumüller, Florian Gebhard, Markus S Huber-Lang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Immunomodulatory and cardio-protective effects of differentially originated multipotent mesenchymal stroma cells during polymicrobial sepsis in mice.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025
    Article
  4. Article
  5. Analysis of Global Research Trends of Trauma-Related Arrhythmias.Open access emergency medicine : OAEM · 2025
    Article
  6. Observational
  7. Article
  8. Mechanisms of Post-critical Illness Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

10 authors at 1 institution in 1 country.

Christian K BraunInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
Miriam KalbitzDepartment of Orthopedic Trauma, Hand-, Plastic- and Reconstructive Surgery, University Hospital of Ulm, Ulm, Germany.
Rebecca HalbgebauerInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
Philipp EiseleInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
David A C MessererInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
Sebastian WeckbachDepartment of Orthopedic Surgery, University Hospital of Ulm, Ulm, Germany.
Anke SchultzeInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
Sonja BraumüllerInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.
Florian GebhardDepartment of Orthopedic Trauma, Hand-, Plastic- and Reconstructive Surgery, University Hospital of Ulm, Ulm, Germany.
Markus S Huber-LangInstitute of Clinical and Experimental Trauma-Immunology, University Hospital of Ulm, Ulm, Germany.ORCID http://orcid.org/0000-0003-2359-6516
University Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence is emerging that systemic inflammation after trauma drives structural and functional impairment of cardiomyocytes and leads to cardiac dysfunction, thus worsening the outcome of polytrauma patients. This study investigates the structural and molecular changes in heart tissue 4 h after multiple injuries with additional hemorrhagic shock using a clinically relevant rodent model of polytrauma. We determined mediators of systemic inflammation (keratinocyte chemoattractant, macrophage chemotactic protein 1), activated complement component C3a and cardiac troponin I in plasma and assessed histological specimen of the mouse heart via standard histomorphology and immunohistochemistry for cellular and subcellular damage and ongoing apoptosis. Further we investigated spatial and quantitative changes of connexin 43 by immunohistochemistry and western blotting. Our results show significantly increased plasma levels of both keratinocyte chemoattractant and cardiac troponin I 4 h after polytrauma and 2 h after induction of hypovolemia. Although we could not detect any morphological changes, immunohistochemical evaluation showed increased level of tissue high-mobility group box 1, which is both a damage-associated molecule and actively released as a danger response signal. Additionally, there was marked lateralization of the cardiac gap-junction protein connexin 43 following combined polytrauma and hemorrhagic shock. These results demonstrate a molecular manifestation of remote injury of cardiac muscle cells in the early phase after polytrauma and hemorrhagic shock with marked disruption of the cardiac gap junction. This disruption of an important component of the electrical conduction system of the heart may lead to arrhythmia and consequently to cardiac dysfunction.

Indexed as

HeartHumansMultiple TraumaShock, Hemorrhagic

Identifiers

PMID29084268
PMCPMC5662170
OpenAlexW2765365439

What OpenQuestion holds

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LicenceCC BY
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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.