Evidence map›Paper›PMID 40533933›Full record

ArticleJournal of cellular and molecular medicine2025

Nicotine Exacerbates Arrhythmogenesis in Rabbit Right Ventricular Outflow Tract Triggered by Chronic Obstructive Pulmonary Disease.

Chao-Shun Chan, Feng-Zhi Lin, Yao-Chang Chen, Satoshi Higa, Shih-Ann Chen, Yi-Jen Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. 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. Research Progress on Animal Models of Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2026
    Review
  2. 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

6 authors.

Chao-Shun ChanDivision of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Feng-Zhi LinGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Yao-Chang ChenDepartment of Biomedical Engineering, National Defense Medical Center, Taipei, Taiwan.
Satoshi HigaCardiac Electrophysiology and Pacing Laboratory, Division of Cardiovascular Medicine, Makiminato Central Hospital, Okinawa, Japan.
Shih-Ann ChenHeart Rhythm Center, Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Yi-Jen ChenDivision of Cardiology, Department of Internal Medicine, Wan-Fang Hospital, Taipei Medical University, Taipei, Taiwan.ORCID 0000-0001-7224-4491

Funding

National Science and Technology Council of Taiwan NSTC 110-2314-B-038-126-MY2National Science and Technology Council of Taiwan NSTC112-2314-B-038-102Taipei Medical University Hospital 111TMUH-MOST-22the Foundation for the Development of Internal Medicine in Okinawa 4-02-004the Foundation for the Development of Internal Medicine in Okinawa 4-02-005
6 · The paper itself

Abstract

Cigarette smoke includes nicotine that increases ventricular tachycardia (VT) risk. Chronic obstructive pulmonary disease (COPD) and right ventricular outflow tract (RVOT) constitute the primary risk factor and origin of VT, respectively. To investigate the arrhythmogenesis of nicotine in COPD, we employed tachypacing with or without H89, KN93 and KB-R7943 treatment, along with patch clamp experiments and Masson's trichrome staining in control rabbits and rabbits with human leukocyte elastase (0.3 unit/kg)-induced COPD. Following 20-Hz tachypacing and isoproterenol treatment, COPD RVOTs had a higher VT incidence than control RVOTs. Nicotine-treated COPD RVOTs had higher ventricular arrhythmogenesis than non-treated COPD RVOTs. VTs induced in COPD and nicotine-treated COPD RVOTs were suppressed by H89, KN93, or KB-R7943. COPD RVOT myocytes exhibited shorter action potentials than control RVOT myocytes; nicotine-treated COPD RVOT myocytes exhibited longer action potentials than COPD RVOT myocytes. Both COPD and nicotine-treated COPD myocytes had smaller L-type Ca

Indexed as

Arrhythmias, CardiacHeart VentriclesNicotinePulmonary Disease, Chronic ObstructiveTachycardia, VentricularAction PotentialsAnimalsCalcium Channels, L-TypeDisease Models, AnimalHumansMaleMyocytes, CardiacRabbitsCalcium Channels, L-TypeNicotinechronic obstructive pulmonary diseasenicotineright ventricular outflow tractventricular tachycardia

Identifiers

PMID40533933
PMCPMC12176695

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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.