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Cardiovascular Research Advance Access first published online on August 20, 2009
This version [Corrected Proof] published online on September 16, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp286
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Effect of N-acetylcysteine on sympathetic hyperinnervation in post-infarcted rat hearts

Tsung-Ming Lee1,2, Po-Yu Lai3 and Nen-Chung Chang2,4,*

1 Cardiology Section, Department of Medicine, Chi-Mei Medical Center, Tainan, Taiwan
2 Department of Internal Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan
3 School of Medicine, Taipei Medical University
4 Cardiology Section, Department of Internal Medicine, Taipei Medical University Hospital, 252, Wu-Hsing St Taipei, Taiwan

* Corresponding author. Tel: +886 2 2737 2181, Fax: +886 2 2736 4222, Email: ncchang{at}tmu.edu.tw

Aims: The purpose of this study was to determine whether N-acetylcysteine (NAC) attenuates cardiac sympathetic hyperinnervation through replenishment of glutathione in infarcted rats.

Methods and results: After ligation of the coronary artery, male Wistar rats were randomized to either vehicle, NAC, or vitamins C + E groups for 4 weeks. Post-infarction was associated with increased oxidant release, as measured by tissue isoprostane and myocardial glutathione. Measurement of myocardial norepinephrine levels revealed a significant elevation in vehicle-treated infarcted rats compared with sham-operated rats. Sympathetic hyperinnervation was blunted after administering NAC, as assessed by immunofluorescent analysis of tyrosine hydroxylase and western blotting and real-time quantitative RT–PCR of nerve growth factor. Arrhythmic scores during programmed stimulation in the vehicle-treated infarcted rats were significantly higher than those in animals treated with NAC. Although NAC and vitamins showed similar effects on ventricular remodelling, only NAC demonstrated beneficial effects on sympathetic hyperinnervation. Furthermore, the effects of NAC on nerve growth factor were abolished by administering L-buthionine sulfoximinem, an inhibitor of {gamma}-glutamylcysteine ligase.

Conclusion: Chronic use of NAC, but not vitamins, after infarction is associated with down-regulation of nerve growth factor proteins, probably through a glutathione-dependent pathway, and thus plays a critical role in the beneficial effect on the arrhythmogenic response to programmed electrical stimulation.

KEYWORDS Glutathione; Myocardial infarction; N-acetylcysteine; Norepinephrine; Sympathetic innervation

Time for primary review: 32 days


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