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Influence of exposure to electromagnetic field on the cardiovascular system

Authors
Jeong, Ji HoonKim, J.S.Lee, B.C.Min, Y.S.Kim, Dong SeokRyu, J.S.Soh, K.S.Seo, K.M.Sohn, Uy Dong
Issue Date
Jan-2005
Keywords
Cardiovascular system; ECG; Electromagnetic field
Citation
Autonomic and Autacoid Pharmacology, v.25, no.1, pp 17 - 23
Pages
7
Journal Title
Autonomic and Autacoid Pharmacology
Volume
25
Number
1
Start Page
17
End Page
23
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/26149
DOI
10.1111/j.1474-8673.2004.00328.x
ISSN
1474-8665
Abstract
We examined whether extremely low frequency electromagnetic fields (ELF-EMF) affect the basal level of cardiovascular parameters and influence of drugs acting on the sympathetic nervous system. Male rats were exposed to sham control and EMF (60 Hz, 20 G) for 1 (MF-1) or 5 days (MF-5). We evaluated the alterations of blood pressure (BP), pulse pressure (PP), heart rate (HR), and the PR interval, QRS interval and QT interval on the electrocardiogram and dysrhythmic ratio in basal level and dysrhythmia induced by β-adrenoceptor agonists. In terms of the basal levels, there were no statistically significant differences among control, MF-1 and MF-5 in PR interval, QRS interval, mean BP, HR and PP. However, the QT interval, representing ventricular repolarization, was significantly reduced by MF-1 (P < 0.05). (-)-Dobutamine (β1-adrenoceptor-selective agonist)-induced tachycardia was significantly suppressed by ELF-EMF exposure in MF-1 for the increase in HR (AHR), the decrease in QRS interval (ΔQRS) and the decrease in QT (ΔQT) interval. Adrenaline (nonselective β-receptor agonist)-induced dysrhythmia was also significantly suppressed by ELF-EMF in MF-1 for the number of missing beats, the dysrhythmic ratio, and the increase in BP and PP. These results indicated that 1-day exposure to ELF-EMF (60 Hz, 20 G) could suppress the increase in HR by affecting ventricular repolarization and may have a down-regulatory effect on responses of the cardiovascular system induced by sympathetic agonists.
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