Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents
BackgroundChronic electronic (e) cigarette users have increased resting cardiac sympathetic nerve activity and increased susceptibility to oxidative stress. The purpose of the present study is to determine the role of nicotine versus non‐nicotine constituents in e‐cigarette emissions in causing thes...
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Format: | Article |
Language: | English |
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Wiley
2017-09-01
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Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
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Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.117.006579 |
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author | Roya S. Moheimani May Bhetraratana Kacey M. Peters Benjamin K. Yang Fen Yin Jeffrey Gornbein Jesus A. Araujo Holly R. Middlekauff |
author_facet | Roya S. Moheimani May Bhetraratana Kacey M. Peters Benjamin K. Yang Fen Yin Jeffrey Gornbein Jesus A. Araujo Holly R. Middlekauff |
author_sort | Roya S. Moheimani |
collection | DOAJ |
description | BackgroundChronic electronic (e) cigarette users have increased resting cardiac sympathetic nerve activity and increased susceptibility to oxidative stress. The purpose of the present study is to determine the role of nicotine versus non‐nicotine constituents in e‐cigarette emissions in causing these pathologies in otherwise healthy humans. Methods and ResultsThirty‐three healthy volunteers who were not current e‐cigarette or tobacco cigarette smokers were studied. On different days, each participant used an e‐cigarette with nicotine, an e‐cigarette without nicotine, or a sham control. Cardiac sympathetic nerve activity was determined by heart rate variability, and susceptibility to oxidative stress was determined by plasma paraoxonase activity. Following exposure to the e‐cigarette with nicotine, but not to the e‐cigarette without nicotine or the sham control, there was a significant and marked shift in cardiac sympathovagal balance towards sympathetic predominance. The decrease in high‐frequency component and the increases in the low‐frequency component and the low‐frequency to high‐frequency ratio were significantly greater following exposure to the e‐cigarette with nicotine compared with exposure to the e‐cigarette without nicotine or to sham control. Oxidative stress, as estimated by plasma paraoxonase, did not increase following any of the 3 exposures. ConclusionsThe acute sympathomimetic effect of e‐cigarettes is attributable to the inhaled nicotine, not to non‐nicotine constituents in e‐cigarette aerosol, recapitulating the same heart rate variability pattern associated with increased cardiac risk in multiple populations with and without known cardiac disease. Evidence of oxidative stress, as estimated by plasma paraoxonase activity, was not uncovered following acute e‐cigarette exposure. |
first_indexed | 2024-04-13T15:35:50Z |
format | Article |
id | doaj.art-c67a86ddc3434724ae1cc9995221a792 |
institution | Directory Open Access Journal |
issn | 2047-9980 |
language | English |
last_indexed | 2024-04-13T15:35:50Z |
publishDate | 2017-09-01 |
publisher | Wiley |
record_format | Article |
series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
spelling | doaj.art-c67a86ddc3434724ae1cc9995221a7922022-12-22T02:41:16ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802017-09-016910.1161/JAHA.117.006579Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine ConstituentsRoya S. Moheimani0May Bhetraratana1Kacey M. Peters2Benjamin K. Yang3Fen Yin4Jeffrey Gornbein5Jesus A. Araujo6Holly R. Middlekauff7David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CADepartment of Biomathematics, David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CADivision of Cardiology Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CABackgroundChronic electronic (e) cigarette users have increased resting cardiac sympathetic nerve activity and increased susceptibility to oxidative stress. The purpose of the present study is to determine the role of nicotine versus non‐nicotine constituents in e‐cigarette emissions in causing these pathologies in otherwise healthy humans. Methods and ResultsThirty‐three healthy volunteers who were not current e‐cigarette or tobacco cigarette smokers were studied. On different days, each participant used an e‐cigarette with nicotine, an e‐cigarette without nicotine, or a sham control. Cardiac sympathetic nerve activity was determined by heart rate variability, and susceptibility to oxidative stress was determined by plasma paraoxonase activity. Following exposure to the e‐cigarette with nicotine, but not to the e‐cigarette without nicotine or the sham control, there was a significant and marked shift in cardiac sympathovagal balance towards sympathetic predominance. The decrease in high‐frequency component and the increases in the low‐frequency component and the low‐frequency to high‐frequency ratio were significantly greater following exposure to the e‐cigarette with nicotine compared with exposure to the e‐cigarette without nicotine or to sham control. Oxidative stress, as estimated by plasma paraoxonase, did not increase following any of the 3 exposures. ConclusionsThe acute sympathomimetic effect of e‐cigarettes is attributable to the inhaled nicotine, not to non‐nicotine constituents in e‐cigarette aerosol, recapitulating the same heart rate variability pattern associated with increased cardiac risk in multiple populations with and without known cardiac disease. Evidence of oxidative stress, as estimated by plasma paraoxonase activity, was not uncovered following acute e‐cigarette exposure.https://www.ahajournals.org/doi/10.1161/JAHA.117.006579electronic cigarettesheart rate variabilitynicotineoxidant stresssympathetic nervous systemtobacco |
spellingShingle | Roya S. Moheimani May Bhetraratana Kacey M. Peters Benjamin K. Yang Fen Yin Jeffrey Gornbein Jesus A. Araujo Holly R. Middlekauff Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease electronic cigarettes heart rate variability nicotine oxidant stress sympathetic nervous system tobacco |
title | Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents |
title_full | Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents |
title_fullStr | Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents |
title_full_unstemmed | Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents |
title_short | Sympathomimetic Effects of Acute E‐Cigarette Use: Role of Nicotine and Non‐Nicotine Constituents |
title_sort | sympathomimetic effects of acute e cigarette use role of nicotine and non nicotine constituents |
topic | electronic cigarettes heart rate variability nicotine oxidant stress sympathetic nervous system tobacco |
url | https://www.ahajournals.org/doi/10.1161/JAHA.117.006579 |
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