Cardiovascular effects of linalyl acetate in acute nicotine exposure
Kim et al. Environmental Health and Preventive Medicine
Cardiovascular effects of linalyl acetate in acute nicotine exposure
Ju Ri Kim 0
Purum Kang 0
Hui Su Lee 0
Ka Young Kim 0 1
Geun Hee Seol 0
0 Department of Basic Nursing Science, School of Nursing, Korea University , Seoul 02841 , Republic of Korea
1 Department of Nursing, School of Nursing, Gachon University , Incheon 21936 , Republic of Korea
Backgroud: Smoking is a risk factor for cardiovascular diseases as well as pulmonary dysfunction. In particular, adolescent smoking has been reported to have a higher latent risk for cardiovascular disease. Despite the risk to and vulnerability of adolescents to smoking, the mechanisms underlying the effects of acute nicotine exposure on adolescents remain unknown. This study therefore evaluated the mechanism underlying the effects of linalyl acetate on cardiovascular changes in adolescent rats with acute nicotine exposure. Methods: Parameters analyzed included heart rate (HR), systolic blood pressure, lactate dehydrogenase (LDH) activity, vascular contractility, and nitric oxide levels. Results: Compared with nicotine alone, those treated with nicotine plus 10 mg/kg (p = 0.036) and 100 mg/kg (p = 0.023) linalyl acetate showed significant reductions in HR. Moreover, the addition of 1 mg/kg (p = 0.011), 10 mg/kg (p = 0.010), and 100 mg/kg (p = 0.011) linalyl acetate to nicotine resulted in significantly lower LDH activity. Nicotine also showed a slight relaxation effect, followed by a sustained recontraction phase, whereas nicotine plus linalyl acetate or nifedipine showed a constant relaxation effect on contraction of mouse aorta (p < 0.001). Furthermore, nicotine-induced increases in nitrite levels were decreased by treatment with linalyl acetate (p < 0.001). Conclusions: Taken together, our findings suggest that linalyl acetate treatment resulted in recovery of cell damage and cardiovascular changes caused by acute nicotine-induced cardiovascular disruption. Our evaluation of the influence of acute nicotine provides potential insights into the effects of environmental tobacco smoke and suggests linalyl acetate as an available mitigating agent.
Linalyl acetate; Acute nicotine; Adolescent; Cardiovascular changes
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Background
Smoking is an independent risk factor for cardiovascular
diseases, including atherosclerosis and ischemic heart
diseases, by virtue of its negative effects on vascular
endothelial function [33, 34] as well as pulmonary
dysfunction [16, 20]. Most studies to date have focused on
the mechanisms and pathophysiology of chronic diseases
caused by smoking [3, 4, 12]. However, acute exposure,
defined as a single exposure to a harmful substance [25],
is an important issue in adolescents who begin to smoke
voluntarily [11]. Adolescents are more vulnerable to
neurobiological changes, mental health, and
substanceuse disorders, as this period of life is essential for brain
development associated with self-control and
regulation [9, 46]. Furthermore, adolescents who smoke have
been reported to be at higher risk for cardiovascular
disease than non-smoking individuals [15], and
vulnerability to nicotine addiction has been reported higher
in adolescents than in adults [14, 17, 35]. Despite the
risks associated with adolescent smoking, the
mechanisms underlying the effects of acute nicotine exposure
on adolescents remain unknown. Animal models,
especially adolescent rats aged 28–42 postnatal days,
have been used to effectively investigate the
pathophysiological effects of nicotine [40, 46].
Nicotine, one of the constituents of cigarettes,
rapidly reaches the blood and brain after being absorbed
through inhalation [2] and is thought to contribute to
cardiovascular diseases caused by cigarette smoking
[8, 28] and possibly the development of atherosclerosis
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
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[21]. The physiological effects of nicotine appear to
differ depending on the dose, duration of exposure,
and method of application [8]. A single exposure to
nicotine has been reported to result in cognitive
impairment, including impairments in learning and
memory [14, 17, 35]. Acute exposure to nicotine has
been reported to increase anxiogenic-like effects in
rats and reduce behavioral pattern organizations, as
shown by T-pattern analysis [5].
Linalyl acetate and linalool, the major constituent of
several aroma essential oils, may regulate cardiovascula (...truncated)