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Low-Level Vagus Nerve Stimulation Reverses Cardiac Dysfunction and Subcellular Calcium Handling in Rats With Post-Myocardial Infarction Heart Failure.
- Source :
-
International heart journal [Int Heart J] 2016 May 25; Vol. 57 (3), pp. 350-5. Date of Electronic Publication: 2016 May 13. - Publication Year :
- 2016
-
Abstract
- 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 Ca(2+) ATPase (SERCA2a), Na(+)-Ca(2+) 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.
- Subjects :
- Animals
Autonomic Nervous System physiopathology
Calcium metabolism
Calcium-Binding Proteins metabolism
Disease Models, Animal
Male
Rats
Rats, Sprague-Dawley
Ryanodine Receptor Calcium Release Channel metabolism
Sodium-Calcium Exchanger metabolism
Treatment Outcome
Ventricular Dysfunction metabolism
Ventricular Dysfunction physiopathology
Ventricular Dysfunction therapy
Heart Failure etiology
Heart Failure metabolism
Heart Failure physiopathology
Heart Failure therapy
Myocardial Infarction complications
Myocytes, Cardiac metabolism
Sarcoplasmic Reticulum Calcium-Transporting ATPases metabolism
Vagus Nerve Stimulation methods
Subjects
Details
- Language :
- English
- ISSN :
- 1349-3299
- Volume :
- 57
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- International heart journal
- Publication Type :
- Academic Journal
- Accession number :
- 27181040
- Full Text :
- https://doi.org/10.1536/ihj.15-516