Cardiovascular effects of linalyl acetate in acute nicotine exposure

Abstract 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 under...

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Main Authors: Ju Ri Kim, Purum Kang, Hui Su Lee, Ka Young Kim, Geun Hee Seol
Format: Article
Language:English
Published: Komiyama Printing Co. Ltd 2017-04-01
Series:Environmental Health and Preventive Medicine
Subjects:
Online Access:http://link.springer.com/article/10.1186/s12199-017-0651-6
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author Ju Ri Kim
Purum Kang
Hui Su Lee
Ka Young Kim
Geun Hee Seol
author_facet Ju Ri Kim
Purum Kang
Hui Su Lee
Ka Young Kim
Geun Hee Seol
author_sort Ju Ri Kim
collection DOAJ
description Abstract 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.
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spelling doaj.art-6728da792aed43dbb6f980dd95d48a722022-12-22T02:13:30ZengKomiyama Printing Co. LtdEnvironmental Health and Preventive Medicine1342-078X1347-47152017-04-012211710.1186/s12199-017-0651-6Cardiovascular effects of linalyl acetate in acute nicotine exposureJu Ri Kim0Purum Kang1Hui Su Lee2Ka Young Kim3Geun Hee Seol4Department of Basic Nursing Science, School of Nursing, Korea UniversityDepartment of Basic Nursing Science, School of Nursing, Korea UniversityDepartment of Basic Nursing Science, School of Nursing, Korea UniversityDepartment of Basic Nursing Science, School of Nursing, Korea UniversityDepartment of Basic Nursing Science, School of Nursing, Korea UniversityAbstract 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.http://link.springer.com/article/10.1186/s12199-017-0651-6Linalyl acetateAcute nicotineAdolescentCardiovascular changes
spellingShingle 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
Linalyl acetate
Acute nicotine
Adolescent
Cardiovascular changes
title Cardiovascular effects of linalyl acetate in acute nicotine exposure
title_full Cardiovascular effects of linalyl acetate in acute nicotine exposure
title_fullStr Cardiovascular effects of linalyl acetate in acute nicotine exposure
title_full_unstemmed Cardiovascular effects of linalyl acetate in acute nicotine exposure
title_short Cardiovascular effects of linalyl acetate in acute nicotine exposure
title_sort cardiovascular effects of linalyl acetate in acute nicotine exposure
topic Linalyl acetate
Acute nicotine
Adolescent
Cardiovascular changes
url http://link.springer.com/article/10.1186/s12199-017-0651-6
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