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Am J Physiol Heart Circ Physiol. 2019 Jun 7. doi: 10.1152/ajpheart.00738.2018. [Epub ahead of print]

Chronic Intermittent Electronic Cigarette Exposure Induces Cardiac Dysfunction and Atherosclerosis in Apolipoprotein E (ApoE) Knockout Mice.

Author information

1
Charles R. Drew University of Medicine and Science, United States.
2
Department of Neurobiology, David Geffen School of Medicine at UCLA, United States.
3
David Geffen School of Medicine at UCLA, United States.
4
Internal Medicine, Charles R. Drew University of Medicine and Science, United States.
5
Endocrinology, Metabolism & Molecular Medicine, Charles R. Drew University of Medicine & Science, UCLA School of Medicine, United States.
6
Physiology, David Geffen School of Medicine at University of California, United States.
7
Internal Medicine, Charles R. Drew Unversity, United States.
8
Charles R. Drew University of Medicine and Science and University of California, Los Angeles, United States.

Abstract

Electronic cigarettes (e-cigarettes), also known as electronic nicotine delivery systems (ENDS) are a popular alternative to conventional nicotine cigarettes, both among smokers and those who have never smoked. In spite of the widespread use of e-cigarettes and the proposed detrimental cardiac and atherosclerotic effects of nicotine, the effects of e-cigarettes on these systems are not known. In this study, we investigated the cardiovascular and cardiac effects of e-cigarettes with and without nicotine in Apolipoprotein E knockout (ApoE-/-) mice. We developed an e-cigarettes exposure model that delivers nicotine in a manner similar to that of human e-cigarettes users. Using commercially available e-cigarettes, bluCig PLUS, ApoE-/- mice were exposed to saline, e-cigarette without nicotine [e-cigarette (0%)] and e-cigarette with 2.4% nicotine [e-cigarette (2.4%)] aerosol for 12 weeks. Echocardiographic data show that mice treated with e-cigarette (2.4%) had decreased left ventricular fractional shortening and ejection fraction compared to e-cigarette (0%) and saline. Ventricular transcriptomic analysis revealed changes in genes associated with metabolism, circadian rhythm and inflammation in e-cigarette (2.4%)-treated ApoE-/- mice. Transmission electron microscopy revealed that cardiomyocytes of mice treated with e-cigarette (2.4%) exhibited ultrastructural abnormalities indicative of cardiomyopathy. Additionally, we observed increased oxidative stress and mitochondrial DNA mutations in mice treated with e-cigarette (2.4%). ApoE-/- mice on e-cigarette (2.4%) had also increased atherosclerotic lesions compared to saline aerosol-treated mice. These results demonstrate adverse effects of e-cigarettes on cardiac function in mice.

KEYWORDS:

Atherosclerosis; Cardiomyopathy; Cardiovascular Disease; Inflammation; Myocardial Biology

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