Evidence map›Paper›PMID 27391645›Full record

ArticlePloS one2016

Dissecting the Effects of Ischemia and Reperfusion on the Coronary Microcirculation in a Rat Model of Acute Myocardial Infarction.

Maurits R Hollander, Guus A de Waard, Lara S F Konijnenberg, Rosalie M E Meijer-van Putten, Charissa E van den Brom, Nanne Paauw, Helga E de Vries, Peter M van de Ven, Jurjan Aman, Geerten P Van Nieuw-Amerongen and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

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  3. Longitudinal [European journal of nuclear medicine and molecular imaging · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 1 institution in 1 country.

Maurits R HollanderDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Guus A de WaardDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Lara S F KonijnenbergDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Rosalie M E Meijer-van PuttenDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Charissa E van den BromInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Nanne PaauwDepartment of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands.
Helga E de VriesDepartment of Molecular Cell Biology and Immunology, VU Medical Center, Amsterdam, The Netherlands.
Peter M van de VenDepartment of Epidemiology and Biostatistics, VU Medical Center, Amsterdam, The Netherlands.
Jurjan AmanInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Geerten P Van Nieuw-AmerongenInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Peter L HordijkInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Hans W M NiessenInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Anton J G HorrevoetsInstitute for Cardiovascular Research, VU Medical Center, Amsterdam, The Netherlands.
Niels Van RoyenDepartment of Cardiology, VU Medical Center, Amsterdam, The Netherlands.
Amsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicrovascular injury (MVI) after coronary ischemia-reperfusion is associated with high morbidity and mortality. Both ischemia and reperfusion are involved in MVI, but to what degree these phases contribute is unknown. Understanding the etiology is essential for the development of new potential therapies. METHODS AND

findingsRats were divided into 3 groups receiving either 30 minutes ischemia, 90 minutes ischemia or 30 minutes ischemia followed by 60 minutes reperfusion. Subsequently hearts were ex-vivo perfused in a Langendorff-model. Fluorescence and electron microscopy was used for analysis of capillary density, vascular permeability and ultrastructure. Most MVI was observed after 30 minutes ischemia followed by 60 minutes reperfusion. In comparison to the 30' and 90' ischemia group, wall thickness decreased (207.0±74 vs 407.8±75 and 407.5±71, p = 0.02). Endothelial nuclei in the 30'-60' group showed irreversible damage and decreased chromatin density variation (50.5±9.4, 35.4±7.1 and 23.7±3.8, p = 0.03). Cell junction density was lowest in the 30'-60' group (0.15±0.02 vs 2.5±0.6 and 1.8±0.7, p<0.01). Microsphere extravasation was increased in both the 90' ischemia and 30'-60' group.

conclusionsIschemia alone for 90 minutes induces mild morphological changes to the coronary microcirculation, with increased vascular permeability. Ischemia for 30 minutes, followed by 60 minutes of reperfusion, induces massive MVI. This shows the direct consequences of reperfusion on the coronary microcirculation. These data imply that a therapeutic window exists to protect the microcirculation directly upon coronary revascularization.

Indexed as

Coronary CirculationAnimalsCapillariesCell CommunicationCell NucleusChromatinDisease Models, AnimalHeartIschemiaMaleMicrospheresMyocardial InfarctionMyocardial ReperfusionMyocardial Reperfusion InjuryPerfusionPermeabilityChromatin

Identifiers

PMID27391645
PMCPMC4938574
OpenAlexW2461872012

What OpenQuestion 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 OpenQuestion graph.