Key result
Long-term electronic cigarette exposure in mice induced cardiovascular dysfunction, including impaired vasodilation, systemic hypertension, and cardiac hypertrophy, similar to tobacco smoking.
Why the study?
Does long-term electronic cigarette exposure induce cardiovascular dysfunction similar to tobacco cigarettes in a mouse model?
Does long-term electronic cigarette exposure induce cardiovascular dysfunction similar to tobacco cigarettes in a mouse model?
Long-term e-cigarette exposure in a mouse model induces cardiovascular dysfunction, including hypertension and cardiac hypertrophy, similar to tobacco smoking.
Answers are grounded in this paper and cite their sources.
May warrant e-cigarette caution akin to smoking; leaves open human cardiovascular translation from mouse model.
A chronic mouse exposure model that mimics human e-cigarette vaping and allows comparison with tobacco cigarette smoking was developed and utilized to perform longitudinal studies of alterations in cardiovascular function. E-cigarette exposure led to the onset of cardiovascular disease similar to that with tobacco cigarette smoking. Impaired endothelium-dependent and endothelium-independent vasodilation with increased adrenergic vasoconstriction were observed, paralleling the onset of systemic hypertension and subsequent cardiac hypertrophy. This cardiovascular toxicity was dependent on exposure duration and nicotine dose.
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Elmahdy et al. (2021) studied Cardiovascular dysfunction. Electronic cigarette exposure vs. Tobacco cigarette smoking was evaluated on Alterations in cardiovascular function (vasodilation, vasoconstriction, hypertension, cardiac hypertrophy). Long-term electronic cigarette exposure in mice induced cardiovascular dysfunction, including impaired vasodilation, systemic hypertension, and cardiac hypertrophy, similar to tobacco smoking.
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