Abstract
BackgroudSmoking 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.MethodsParameters analyzed included heart rate (HR), systolic blood pressure, lactate dehydrogenase (LDH) activity, vascular contractility, and nitric oxide levels.ResultsCompared 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).ConclusionsTaken 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.
Highlights
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]
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 heart rate (HR)
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 lactate dehydrogenase (LDH) activity
Summary
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]. 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. 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]
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