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Cardiovascular Research Advance Access originally published online on December 7, 2007
Cardiovascular Research 2008 77(4):713-721; doi:10.1093/cvr/cvm092
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Modulation of the myocardial redox state by vagal nerve stimulation after experimental myocardial infarction

Takaki Tsutsumi1, Tomomi Ide1,*, Mayumi Yamato2, Wataru Kudou2, Makoto Andou1, Yoshitaka Hirooka1, Hideo Utsumi3, Hiroyuki Tsutsui4 and Kenji Sunagawa1

1 Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
2 Department of REDOX Medicinal Science, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan
3 Laboratory of Bio-function Analysis, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan
4 Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan

* Corresponding author. Tel: +81 92 642 5360; fax: +81 92 642 5374. E-mail address: tomom_i{at}cardiol.med.kyushu-u.ac.jp

Aims: Redox alteration plays a major role in the pathogenesis of heart failure (HF). Since vagal nerve stimulation (VNS) is known to improve survival and attenuate cardiac remodelling, we hypothesized that VNS may modulate the myocardial redox state.

Methods and results: Using a chronic HF mouse model, we applied VNS for 15 min and measured myocardial redox status using in vivo electron spin resonance spectroscopy. Signal decay rate of the nitroxyl probe, an index of redox status, was enhanced in HF compared with sham (0.16 ± 0.01 vs. 0.13 ± 0.01 min–1, P < 0.05; n = 6), and VNS normalized this enhancement (0.13 ± 0.01 min–1, P < 0.05). Atropine sulphate abolished the VNS effects, indicating that the VNS modulates myocardial redox state via muscarinic receptors. N{omega}-Nitro-L-arginine methyl ester treatment and fixed-rate atrial pacing showed a trend to suppress the VNS effects, suggesting the involvement of nitric oxide-based signalling and myocardial oxygen consumption. Moreover, VNS decreased the myocardial norepinephrine (NE) level (0.25 ± 0.07 vs. 0.60 ± 0.12 ng/mL, P < 0.05; n = 6). Reactive oxygen species production from cultured cardiomyocytes was enhanced by β-adrenergic activation, which was partially antagonized by 10 µmol/L acetylcholine (ACh) (relative value compared with control: NE 3.7 ± 0.5, NE + ACh 2.5 ± 0.3, P < 0.05; n = 12).

Conclusion: The present study suggests that VNS modulates the cardiac redox status and adrenergic drive, and thereby suppresses free radical generation in the failing heart.

KEYWORDS Autonomic nervous system; Acetylcholine; Heart failure; Oxidative stress

Time for primary review: 13 days


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