Low-Level Vagus Nerve Stimulation Reverses Cardiac Dysfunction and Subcellular Calcium Handling in Rats With Post-Myocardial Infarction Heart Failure
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- Zhang Yunhe
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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- Chen Ao
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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- Song Lei
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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- Li Min
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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- Luo Zhangyuan
- Ensense Biomedical Technologies (Shanghai) Co., Ltd
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- Zhang Wenzan
- Ensense Biomedical Technologies (Shanghai) Co., Ltd
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- Chen Yingmin
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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- He Ben
- Department of Cardiology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University
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抄録
Vagus nerve stimulation (VNS), targeting the imbalanced autonomic nervous system, is a promising therapeutic approach for chronic heart failure (HF). Moreover, calcium cycling is an important part of cardiac excitation-contraction coupling (ECC), which also participates in the antiarrhythmic effects of VNS. We hypothesized that low-level VNS (LL-VNS) could improve cardiac function by regulation of intracellular calcium handling properties. The experimental HF model was established by ligation of the left anterior descending coronary artery (LAD). Thirty-two male Sprague-Dawley rats were divided into 3 groups as follows; control group (sham operated without coronary ligation, n = 10), HF-VNS group (HF rats with VNS, n = 12), and HF-SS group (HF rats with sham nerve stimulation, n = 10). After 8 weeks of treatment, LL-VNS significantly improved left ventricular ejection fraction (LVEF) and attenuated myocardial interstitial fibrosis in the HF-VNS group compared with the HF-SS group. Elevated plasma norepinephrine and dopamine, but not epinephrine, were partially reduced by LL-VNS. Additionally, LL-VNS restored the protein and mRNA levels of sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), Na+–Ca2+ exchanger 1 (NCX1), and phospholamban (PLB) whereas the expression of ryanodine receptor 2 (RyR2) as well as mRNA level was unaffected. Thus, our study results suggest that the improvement of cardiac performance by LL-VNS is accompanied by the reversal of dysfunctional calcium handling properties including SERCA2a, NCX1, and PLB which may be a potential molecular mechanism of VNS for HF.
収録刊行物
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- International Heart Journal
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International Heart Journal 57 (3), 350-355, 2016
一般社団法人 インターナショナル・ハート・ジャーナル刊行会