Evidence map›Paper›PMID 36319860›Full record

ArticleEuropean journal of trauma and emergency surgery : official publication of the European Trauma Society2023

Hemorrhagic shock and tissue injury provoke distinct components of trauma-induced coagulopathy in a swine model.

Alexis L Cralley, Ernest E Moore, Julia R Coleman, Navin Vigneshwar, Matt Bartley, Daniel Kissau, Andrew Eitel, Patrick Hom, Sanchayita Mitra, Arsen Ghasabyan and 9 more

Open access · greenAbstract read
In one paragraph

Article in European journal of trauma and emergency surgery : official publication of the European Trauma Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Characterization of the binding of skeletal muscle myosin to fibrin in trauma.The journal of trauma and acute care surgery · 2026
    Article
  2. Review
  3. Article
  4. siRNA-mediated reduction of a circulating protein in swine using lipid nanoparticles.Molecular therapy. Methods & clinical development · 2024
    Article
  5. 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

19 authors at 5 institutions in 1 country.

Alexis L CralleyDepartment of Surgery, University of Colorado, Aurora, CO, USA. alexis.cralley@cuanschutz.edu.ORCID http://orcid.org/0000-0003-4021-7565
Ernest E MooreDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Julia R ColemanDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Navin VigneshwarDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Matt BartleyDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Daniel KissauDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Andrew EitelDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Patrick HomDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Sanchayita MitraDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Arsen GhasabyanDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Miguel FragosoDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Zihan GuoDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA.
Hiroshi DeguchiDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA.
John H GriffinDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA.
Mitchell J CohenDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Christopher C SillimanVitalant Research Institute, Denver, CO, USA.
Anirban BanerjeeDepartment of Surgery, University of Colorado, Aurora, CO, USA.
Kirk HansenDepartment of Proteomics and Metabolomics, University of Colorado, Aurora, CO, USA.
Angela SauaiaDepartment of Health Systems, Management and Policy, School of Public Health, University of Colorado Denver, Aurora, CO, USA.
University of Colorado Anschutz Medical Campus · USScripps Research Institute · USColorado School of Public Health · USDenver Health Medical Center · USVitalant · US

Funding

Analysis and Characterization of Trauma-Induced CoagulopathyUM1HL120877 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI MORRISSEY, JAMES H., WISNIEWSKI, STEPHEN R · 2013 to 2019
$26.6M
Resuscitation Strategies for Achieving Thrombo-inflammatory HomeostasisRM1GM131968 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI COHEN, MITCHELL, D'ALESSANDRO, ANGELO · 2019 to 2023
$11.3M
Regulation of Protein C PathwaysR01HL142975 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI GRIFFIN, JOHN H, MOSNIER, LAURENT OLIVIER · 2018 to 2025
$7.3M
Mechanisms of Trauma-Induced CoagulopathyT32GM008315 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI Mitchell Cohen, ELIZABETH J. KOVACS · 1991 to 2026
$7.1M
NHLBI NIH HHS R01 HL142975NHLBI NIH HHS UM1 HL120877NIGMS NIH HHS RM1 GM131968NIGMS NIH HHS T32 GM008315
6 · The paper itself

Abstract

introductionTissue injury (TI) and hemorrhagic shock (HS) are the major contributors to trauma-induced coagulopathy (TIC). However, the individual contributions of these insults are difficult to discern clinically because they typically coexist. TI has been reported to release procoagulants, while HS has been associated with bleeding. We developed a large animal model to isolate TI and HS and characterize their individual mechanistic pathways. We hypothesized that while TI and HS are both drivers of TIC, they provoke different pathways; specifically, TI reduces time to clotting, whereas, HS decreases clot strength stimulates hyperfibrinolysis.

methodsAfter induction of general anesthesia, 50 kg male, Yorkshire swine underwent isolated TI (bilateral muscle cutdown of quadriceps, bilateral femur fractures) or isolated HS (controlled bleeding to a base excess target of - 5 mmol/l) and observed for 240 min. Thrombelastography (TEG), calcium levels, thrombin activatable fibrinolysis inhibitor (TAFI), protein C, plasminogen activator inhibitor 1 (PAI-1), and plasminogen activator inhibitor 1/tissue-type plasminogen activator complex (PAI-1-tPA) were analyzed at pre-selected timepoints. Linear mixed models for repeated measures were used to compare results throughout the model.

resultsTI resulted in elevated histone release which peaked at 120 min (p = 0.02), and this was associated with reduced time to clot formation (R time) by 240 min (p = 0.006). HS decreased clot strength at time 30 min (p = 0.003), with a significant decline in calcium (p = 0.001). At study completion, HS animals had elevated PAI-1 (p = 0.01) and PAI-1-tPA (p = 0.04), showing a trend toward hyperfibrinolysis, while TI animals had suppressed fibrinolysis. Protein C, TAFI and skeletal myosin were not different among the groups.

conclusionIsolated injury in animal models can help elucidate the mechanistic pathways leading to TIC. Our results suggest that isolated TI leads to early histone release and a hypercoagulable state, with suppressed fibrinolysis. In contrast, HS promotes poor clot strength and hyperfibrinolysis resulting in hypocoagulability.

Indexed as

Blood Coagulation DisordersShock, HemorrhagicAnimalsCalciumFibrinolysisHemorrhageHistonesMalePlasminogen Activator Inhibitor 1Protein CSwineThrombelastographyCalciumHistonesPlasminogen Activator Inhibitor 1Protein CFibrinolysisHemorrhagic shock animal modelsTissue injuryTrauma-induced coagulopathy

Identifiers

PMID36319860
PMCPMC10802987
OpenAlexW4307805251

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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.