Cardiovascular effects of linalyl acetate in acute nicotine exposure

Environmental Health and Preventive Medicine, Apr 2017

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.

A PDF file should load here. If you do not see its contents the file may be temporarily unavailable at the journal website or you do not have a PDF plug-in installed and enabled in your browser.

Alternatively, you can download the file locally and open with any standalone PDF reader:

https://link.springer.com/content/pdf/10.1186%2Fs12199-017-0651-6.pdf

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 - 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 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. [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)


This is a preview of a remote PDF: https://link.springer.com/content/pdf/10.1186%2Fs12199-017-0651-6.pdf

Ju Ri Kim, Purum Kang, Hui Su Lee, Ka Young Kim, Geun Hee Seol. Cardiovascular effects of linalyl acetate in acute nicotine exposure, Environmental Health and Preventive Medicine, 2017, pp. 42, Volume 22, Issue 1, DOI: 10.1186/s12199-017-0651-6