Evidence map›Paper›PMID 38844477›Full record

ArticleScientific reports2024

Leukocyte filtration and leukocyte modulation therapy during extracorporeal cardiopulmonary resuscitation in a porcine model of prolonged cardiac arrest.

Jensyn J VanZalen, Takahiro Nakashima, Annie Phillips, Joseph E Hill, Angela J Westover, Liandi Lou, Jinhui Liao, Joshua Mergos, Garrett Fogo, Thomas H Sanderson and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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

16 authors.

Jensyn J VanZalenDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Takahiro NakashimaDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Annie PhillipsDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Joseph E HillDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Angela J WestoverDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Liandi LouDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Jinhui LiaoThe Max Harry Weil Institute for Critical Care Research and Innovation, University of Michigan, Ann Arbor, MI, 48109, USA.
Joshua MergosMovement Science, University of Michigan School of Kinesiology, Ann Arbor, MI, 48109, USA.
Garrett FogoThe Max Harry Weil Institute for Critical Care Research and Innovation, University of Michigan, Ann Arbor, MI, 48109, USA.
Thomas H SandersonThe Max Harry Weil Institute for Critical Care Research and Innovation, University of Michigan, Ann Arbor, MI, 48109, USA.
William C StaceyMovement Science, University of Michigan School of Kinesiology, Ann Arbor, MI, 48109, USA.
Mohamad Hakam TibaThe Max Harry Weil Institute for Critical Care Research and Innovation, University of Michigan, Ann Arbor, MI, 48109, USA.
David H HumesDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Robert H BartlettDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Alvaro Rojas-PeñaDepartment of Surgery and ECLS Laboratory, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Robert W NeumarThe Max Harry Weil Institute for Critical Care Research and Innovation, University of Michigan, Ann Arbor, MI, 48109, USA. neumar@umich.edu.

Funding

ECPR After Prolonged Cardiac Arrest: Targeting Mechanisms of the No-ReflowR01HL133129 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BARTLETT, ROBERT H., NEUMAR, ROBERT W. · 2017 to 2020
$3.1M
NHLBI NIH HHS R01 HL133129NIH HHS R01HL133129
6 · The paper itself

Abstract

Extracorporeal cardiopulmonary resuscitation (ECPR) is emerging as a feasible and effective rescue strategy for prolonged cardiac arrest (CA). However, prolonged total body ischemia and reperfusion can cause microvascular occlusion that prevents organ reperfusion and recovery of function. One hypothesized mechanism of microvascular "no-reflow" is leukocyte adhesion and formation of neutrophil extracellular traps. In this study we tested the hypothesis that a leukocyte filter (LF) or leukocyte modulation device (L-MOD) could reduce NETosis and improve recovery of heart and brain function in a swine model of prolonged cardiac arrest treated with ECPR. Thirty-six swine (45.5 ± 2.5 kg, evenly distributed sex) underwent 8 min of untreated ventricular fibrillation CA followed by 30 min of mechanical CPR with subsequent 8 h of ECPR. Two females were later excluded from analysis due to CPR complications. Swine were randomized to standard care (Control group), LF, or L-MOD at the onset of CPR. NET formation was quantified by serum dsDNA and citrullinated histone as well as immunofluorescence staining of the heart and brain for citrullinated histone in the microvasculature. Primary outcomes included recovery of cardiac function based on cardiac resuscitability score (CRS) and recovery of neurologic function based on the somatosensory evoked potential (SSEP) N20 cortical response. In this model of prolonged CA treated with ECPR we observed significant increases in serum biomarkers of NETosis and immunohistochemical evidence of microvascular NET formation in the heart and brain that were not reduced by LF or L-MOD therapy. Correspondingly, there were no significant differences in CRS and SSEP recovery between Control, LF, and L-MOD groups 8 h after ECPR onset (CRS = 3.1 ± 2.7, 3.7 ± 2.6, and 2.6 ± 2.6 respectively; p = 0.606; and SSEP = 27.9 ± 13.0%, 36.7 ± 10.5%, and 31.2 ± 9.8% respectively, p = 0.194). In this model of prolonged CA treated with ECPR, the use of LF or L-MOD therapy during ECPR did not reduce microvascular NETosis or improve recovery of myocardial or brain function. The causal relationship between microvascular NETosis, no-reflow, and recovery of organ function after prolonged cardiac arrest treated with ECPR requires further investigation.

Indexed as

Cardiopulmonary ResuscitationDisease Models, AnimalHeart ArrestAnimalsExtracellular TrapsExtracorporeal Membrane OxygenationFemaleLeukocyte Reduction ProceduresLeukocytesMaleSwineAnimal modelsCardiac arrestExtracorporeal cardiopulmonary resuscitationInflammationLeukocyte modulationNETosisNeutrophil extracellular traps

Identifiers

PMID38844477
PMCPMC11156900

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.