Evidence map›Paper›PMID 42474680›Full record

ArticleIntensive care medicine experimental2026

In vivo mitochondrial oxygen consumption during LPS-induced endotoxemia: a controlled experimental study in swine.

Calvin Jay de Wijs, Jan van den Brink, Patricia A C Specht, Mariëlle van der Kaaij, Harold N J Raat, Bülent Ergin, Robert Jan Stolker, Egbert G Mik, Floor A Harms

Abstract read
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In one paragraph

Article in Intensive care medicine experimental, 2026. 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
–field-weighted citation impact
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.

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

9 authors.

Calvin Jay de WijsLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands. c.dewijs@erasmusmc.nl.ORCID http://orcid.org/0009-0001-5072-3405
Jan van den BrinkLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Patricia A C SpechtLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Mariëlle van der KaaijLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Harold N J RaatLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Bülent ErginLaboratory of Translational Intensive Care, Department of Intensive Care Adult, Erasmus, Rotterdam, MC, the Netherlands.
Robert Jan StolkerLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Egbert G MikLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.
Floor A HarmsLaboratory of Experimental Anesthesiology, Department of Anesthesiology, Erasmus MC, PO Box 2040, 3000 CA , Rotterdam, the Netherlands.

Funding

Nederlandse Vereniging voor Anesthesiologie NVA Young Investigator Grant 2016
6 · The paper itself

Abstract

backgroundSepsis and septic shock are life-threatening syndromes characterized by complex systemic effects, including alterations in tissue oxygenation, mitochondrial function, and organ performance. Despite advances in supportive care, management remains challenging and is largely focused on maintaining adequate perfusion through fluids and vasoactive agents. To better characterize early systemic responses to endotoxemia under different hemodynamic conditions, this study used a swine lipopolysaccharide (LPS)-induced endotoxemia model with graded hypotension exposure. Animals were allocated to a control group (MAP maintained > 80 mmHg) and two LPS-groups defined by different MAP thresholds for initiating hemodynamic support (LPS-1: <80 mmHg; LPS-2: <65 mmHg), with a focus on early mitochondrial and microcirculatory (dys)function.

resultsLPS administration induced marked systemic responses, including tachycardia, metabolic stress, and organ dysfunction. Microcirculatory alterations were present but quantitatively modest. In vivo mitochondrial oxygen tension (mitoPO

conclusionEarly LPS-induced endotoxemia was associated with reduced or blunted mitoVO

Indexed as

EndotoxemiaLactateMicrocirculationMitochondriaRenal injurySwine

Identifiers

PMID42474680
PMCPMC13385532

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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.