Evidence map›Paper›PMID 26918767›Full record

ArticlePloS one2016

Therapeutic Effects of Procainamide on Endotoxin-Induced Rhabdomyolysis in Rats.

Chih-Chin Shih, Hiong-Ping Hii, Cheng-Ming Tsao, Shiu-Jen Chen, Shuk-Man Ka, Mei-Hui Liao, Chin-Chen Wu

Open access · goldAbstract readComparative Study
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. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. DNA methylation alterations in muscle of critically ill patients.Journal of cachexia, sarcopenia and muscle · 2022
    Trial
  3. Article
  4. Review
  5. Article
  6. 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

7 authors at 3 institutions in 1 country.

Chih-Chin ShihGraduate Institute of Medical Sciences, National Defense Medical Center, Taipei, R.O.C., Taiwan.
Hiong-Ping HiiDepartment of Surgery, Chi Mei Medical Center, Tainan, R.O.C., Taiwan.
Cheng-Ming TsaoDepartment of Anesthesiology, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, R.O.C., Taiwan.
Shiu-Jen ChenDepartment of Physiology, National Defense Medical Center, Taipei, R.O.C., Taiwan.
Shuk-Man KaGraduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, R.O.C., Taiwan.
Mei-Hui LiaoDepartment of Pharmacology, National Defense Medical Center, Taipei, R.O.C., Taiwan.
Chin-Chen WuDepartment of Pharmacology, National Defense Medical Center, Taipei, R.O.C., Taiwan.
National Defense Medical Center · TWChi Mei Medical Center · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overt systemic inflammatory response is a predisposing mechanism for infection-induced skeletal muscle damage and rhabdomyolysis. Aberrant DNA methylation plays a crucial role in the pathophysiology of excessive inflammatory response. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1) used to alleviate DNA hypermethylation. Therefore, we evaluated the effects of procainamide on the syndromes and complications of rhabdomyolysis rats induced by lipopolysaccharide (LPS). Rhabdomyolysis animal model was established by intravenous infusion of LPS (5 mg/kg) accompanied by procainamide therapy (50 mg/kg). During the experimental period, the changes of hemodynamics, muscle injury index, kidney function, blood gas, blood electrolytes, blood glucose, and plasma interleukin-6 (IL-6) levels were examined. Kidneys and lungs were exercised to analyze superoxide production, neutrophil infiltration, and DNMTs expression. The rats in this model showed similar clinical syndromes and complications of rhabdomyolysis including high levels of plasma creatine kinase, acute kidney injury, hyperkalemia, hypocalcemia, metabolic acidosis, hypotension, tachycardia, and hypoglycemia. The increases of lung DNMT1 expression and plasma IL-6 concentration were also observed in rhabdomyolysis animals induced by LPS. Treatment with procainamide not only inhibited the overexpression of DNMT1 but also diminished the overproduction of IL-6 in rhabdomyolysis rats. In addition, procainamide improved muscle damage, renal dysfunction, electrolytes disturbance, metabolic acidosis, hypotension, and hypoglycemia in the rats with rhabdomyolysis. Moreover, another DNMT inhibitor hydralazine mitigated hypoglycemia, muscle damage, and renal dysfunction in rhabdomyolysis rats. These findings reveal that therapeutic effects of procainamide could be based on the suppression of DNMT1 and pro-inflammatory cytokine in endotoxin-induced rhabdomyolysis.

Indexed as

AcidosisAnimalsBicarbonatesBiomarkersCreatinineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADNA Methyltransferase 3BDrug Evaluation, PreclinicalElectrolytesEndotoxemiaEndotoxinsHydralazineHypertensionBicarbonatesBiomarkersCreatinineDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADNA Methyltransferase 3BDnmt1 protein, ratElectrolytesendotoxin, Escherichia coliEndotoxinsHydralazineInterleukin-6ProcainamideSuperoxides

Identifiers

PMID26918767
PMCPMC4769298
OpenAlexW2279317522

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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 OpenQuestion graph.