Evidence map›Paper›PMID 27510990›Full record

ArticleCritical care (London, England)2016

Impaired Ca(2+) release contributes to muscle weakness in a rat model of critical illness myopathy.

Monica Llano-Diez, Arthur J Cheng, William Jonsson, Niklas Ivarsson, Håkan Westerblad, Vic Sun, Nicola Cacciani, Lars Larsson, Joseph Bruton

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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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 at 1 institution in 1 country.

Monica Llano-DiezDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Arthur J ChengDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
William JonssonDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Niklas IvarssonDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Håkan WesterbladDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Vic SunDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Nicola CaccianiDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Lars LarssonDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden.
Joseph BrutonDepartment of Physiology & Pharmacology, Karolinska Institutet, von Eulers väg, 8, 2 floor, Stockholm, 171 77, Sweden. joseph.bruton@ki.se.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCritical illness myopathy is an acquired skeletal muscle disorder with severe myosin loss and muscle weakness frequently seen in intensive care unit (ICU) patients. It is unknown if impaired excitation-contraction coupling contributes to the muscle weakness.

methodsWe used a unique ICU model where rats were deeply sedated, post-synaptically pharmacologically paralyzed, mechanically ventilated and closely monitored for up to ten days. Single intact fibers from the flexor digitorum brevis muscle were isolated and used to measure force and free myoplasmic [Ca(2+)] ([Ca(2+)]i) during tetanic contractions.

resultsFibers from ICU rats had 80 % lower tetanic [Ca(2+)]i and produced only 15 % of the force seen in fibers from sham-operated (SHAM) rats. In the presence of 5 mM caffeine, tetanic [Ca(2+)]i was similar in fibers from ICU and SHAM rats but force was 50 % lower in fibers from ICU rats than SHAM rats. Confocal imaging showed disrupted tetanic [Ca(2+)]i transients in fibers from ICU rats compared to SHAM rats. Western blots showed similar levels of Na(+) channel and dihydropyridine receptor (DHPR) protein expression, whereas ryanodine receptor (RyR) and sarco-endoplasmic reticulum Ca(2+) ATPase 1 (SERCA1) expression was markedly lower in muscle of ICU rats than in SHAM rats. Immunohistochemical analysis showed that distribution of Na(+) channel and DHPR protein on the sarcolemma was disrupted in fibers from ICU rats compared with SHAM rats.

conclusionsThese results suggest that impaired SR Ca(2+) release contributes to the muscle weakness seen in patients in ICU.

Indexed as

AnimalsCritical IllnessDisease Models, AnimalEdetic AcidFemaleMaleMuscle ContractionMuscle StrengthMuscle WeaknessMuscular DiseasesRatsRats, Sprague-DawleyEdetic AcidCa2+ handlingCritical illness myopathyExcitation-contraction couplingIntensive care unitSkeletal muscle weakness

Identifiers

PMID27510990
PMCPMC5050561
OpenAlexW2502029340

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.