Evidence map›Paper›PMID 41398534›Full record

ArticleIntensive care medicine experimental2025

Effects of perioperative dexmedetomidine on renal vascular function and renovascular histopathology in ovine cardiopulmonary bypass.

Ashenafi H Betrie, Alemayehu H Jufar, Roger G Evans, Andrew D Cochrane, Bruno Marino, Ian Birchall, Sally G Hood, Peter R McCall, Scott Ayton, Lachlan F Miles and 2 more

Abstract read
In one paragraph

Article in Intensive care medicine experimental, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Ashenafi H BetrieFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Alemayehu H JufarFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Roger G EvansFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Andrew D CochraneFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Bruno MarinoCellsaving and Perfusion Resources, Melbourne, VIC, Australia.
Ian BirchallFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Sally G HoodFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Peter R McCallDepartment of Anaesthesia, Austin Hospital, Melbourne, Australia.
Scott AytonFlorey Department of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Lachlan F MilesFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Clive N MayFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
Yugeesh R LankadevaFlorey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia. yugeesh.lankadeva@florey.edu.au.ORCID http://orcid.org/0000-0002-3589-9111

Funding

National Health and Medical Research Council GNT1122455National Health and Medical Research Council GNT1185777National Health and Medical Research Council GNT2025266National Heart Foundation of Australia NHF105666National Heart Foundation of Australia VG104674
6 · The paper itself

Abstract

backgroundCardiopulmonary bypass (CPB) is integral to the conduct of cardiac surgery but is associated with postoperative acute kidney injury (AKI). Dexmedetomidine, an α₂-adrenoceptor agonist with anti-inflammatory and sympatholytic properties, has putative renoprotective effects. In a recent meta-analysis, dexmedetomidine during CPB reduced AKI; conversely, a large, randomised trial reported an increase in postoperative AKI. Further, we found increased renal tubular injury in sheep receiving dexmedetomidine during CPB. Here, we aimed to determine whether dexmedetomidine during CPB induces changes in renal vascular reactivity or endothelial integrity that could explain focal renal tubular injury.

methodsFourteen instrumented Merino ewes underwent 2 h of non-pulsatile CPB (flow 70 mL/kg/min; MAP 65-75 mmHg; cooled by 3 °C) under standardised propofol-fentanyl-sevoflurane anaesthesia. Animals were randomly allocated to dexmedetomidine (0.4-0.8 µg/kg/h, n = 7) or fluid-matched saline (n = 7) from induction of anesthesia to end-CPB. Arterial pressure, renal blood flow, cortical and medullary perfusion and PO₂ were measured in vivo (n = 7/group). Post-CPB, renal interlobar arteries were isolated for wire myography. Due to standardisation failures, in vitro analyses of dose-response curves for phenylephrine were performed in n = 6 per group, while endothelial-dependent and independent relaxation responses were performed in n = 7 per group. Endothelial histology of CPB arteries was compared with arteries from a separate cohort of healthy Merino ewes (n = 7).

resultsIn vitro functional investigations demonstrated that interlobar arteries from dexmedetomidine-treated sheep exhibited a 2.3-fold increase in phenylephrine sensitivity (pEC₅₀ 5.82 ± 0.27 vs. 5.45 ± 0.23; p = 0.034), with unchanged maximal contraction. Endothelium-dependent and independent relaxations were similar between groups, though inhibitor studies indicated a shift towards cyclooxygenase-mediated dilation under dexmedetomidine. Histology revealed intact endothelial architecture and no damage to endothelial integrity in all groups.

conclusionsPerioperative dexmedetomidine during CPB enhanced α₁-adrenergic vasoconstrictor sensitivity in renal interlobar arteries without disrupting endothelial integrity or compromising renal blood flow or intrarenal perfusion. The enhanced vasoreactivity may contribute to focal renal ischaemia and tubular injury during CPB, which cannot be detected by in vivo measurements of global and regional kidney perfusion and oxygenation. Further investigation is warranted to elucidate the pathways through which dexmedetomidine contributes to renal tubular injury during CPB.

Indexed as

Acute kidney injuryCardiopulmonary bypassCPBDexmedetomidineRenal interlobar arteriesSheepVasoconstriction

Identifiers

PMID41398534
PMCPMC12705920

What Socratic holds

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LicenceCC BY
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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 Socratic graph.