<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Carll AP</submitter><funding>U.S. Department of Health &amp; Human Services | NIH | National Institute of General Medical Sciences (NIGMS)</funding><funding>NHLBI NIH HHS</funding><funding>U.S. Department of Health &amp; Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)</funding><funding>NIGMS NIH HHS</funding><pagination>6088</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9596490</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>E-cigarette use has surged, but the long-term health effects remain unknown. E-cigarette aerosols containing nicotine and acrolein, a combustion and e-cigarette byproduct, may impair cardiac electrophysiology through autonomic imbalance. Here we show in mouse electrocardiograms that acute inhalation of e-cigarette aerosols disturbs cardiac conduction, in part through parasympathetic modulation. We demonstrate that, similar to acrolein or combustible cigarette smoke, aerosols from e-cigarette solvents (vegetable glycerin and propylene glycol) induce bradycardia, bradyarrhythmias, and elevations in heart rate variability during inhalation exposure, with inverse post-exposure effects. These effects are slighter with tobacco- or menthol-flavored aerosols containing nicotine, and in female mice</pubmed_abstract><journal>Nature communications</journal><pubmed_title>E-cigarettes and their lone constituents induce cardiac arrhythmia and conduction defects in mice.</pubmed_title><pmcid>PMC9596490</pmcid><funding_grant_id>P30 GM127607</funding_grant_id><funding_grant_id>P30GM127607</funding_grant_id><funding_grant_id>R01 HL163818</funding_grant_id><funding_grant_id>R01HL147343</funding_grant_id><funding_grant_id>R01HL163818</funding_grant_id><funding_grant_id>R01 HL147343</funding_grant_id><funding_grant_id>R01HL122676</funding_grant_id><funding_grant_id>P50 HL120163</funding_grant_id><funding_grant_id>U54HL120163</funding_grant_id><funding_grant_id>R01 HL122676</funding_grant_id><funding_grant_id>U54 HL120163</funding_grant_id><pubmed_authors>Miles MD</pubmed_authors><pubmed_authors>Theis WS</pubmed_authors><pubmed_authors>Bhatnagar A</pubmed_authors><pubmed_authors>Salatini R</pubmed_authors><pubmed_authors>Shirk GA</pubmed_authors><pubmed_authors>Riggs DW</pubmed_authors><pubmed_authors>Nystoriak MA</pubmed_authors><pubmed_authors>Conklin DJ</pubmed_authors><pubmed_authors>Arab C</pubmed_authors><pubmed_authors>Carll AP</pubmed_authors><pubmed_authors>Fulghum KL</pubmed_authors><pubmed_authors>Talebi N</pubmed_authors></additional><is_claimable>false</is_claimable><name>E-cigarettes and their lone constituents induce cardiac arrhythmia and conduction defects in mice.</name><description>E-cigarette use has surged, but the long-term health effects remain unknown. E-cigarette aerosols containing nicotine and acrolein, a combustion and e-cigarette byproduct, may impair cardiac electrophysiology through autonomic imbalance. Here we show in mouse electrocardiograms that acute inhalation of e-cigarette aerosols disturbs cardiac conduction, in part through parasympathetic modulation. We demonstrate that, similar to acrolein or combustible cigarette smoke, aerosols from e-cigarette solvents (vegetable glycerin and propylene glycol) induce bradycardia, bradyarrhythmias, and elevations in heart rate variability during inhalation exposure, with inverse post-exposure effects. These effects are slighter with tobacco- or menthol-flavored aerosols containing nicotine, and in female mice</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2025-04-18T21:22:31.065Z</modification><creation>2025-04-07T09:17:32.018Z</creation></dates><accession>S-EPMC9596490</accession><cross_references><pubmed>36284091</pubmed><doi>10.1038/s41467-022-33203-1</doi></cross_references></HashMap>