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

التفاصيل البيبلوغرافية
العنوان: Modulation of the myocardial redox state by vagal nerve stimulation after experimental myocardial infarction
المؤلفون: Takaki Tsutsumi, Makoto Andou, Mayumi Yamato, Hideo Utsumi, Yoshitaka Hirooka, Wataru Kudou, Hiroyuki Tsutsui, Tomomi Ide, Kenji Sunagawa
المصدر: Cardiovascular Research. 77:713-721
بيانات النشر: Oxford University Press (OUP), 2007.
سنة النشر: 2007
مصطلحات موضوعية: Male, medicine.medical_specialty, Sympathetic Nervous System, Physiology, Myocardial Infarction, Adrenergic, Muscarinic Antagonists, Nitric Oxide, medicine.disease_cause, Nitric oxide, Mice, Norepinephrine, chemistry.chemical_compound, Oxygen Consumption, Physiology (medical), Internal medicine, Receptors, Adrenergic, beta, Muscarinic acetylcholine receptor, Animals, Medicine, Myocytes, Cardiac, Sulfhydryl Compounds, Enzyme Inhibitors, Cells, Cultured, Heart Failure, business.industry, Myocardium, Cardiac Pacing, Artificial, Electron Spin Resonance Spectroscopy, NADPH Oxidases, Heart, Vagus Nerve, medicine.disease, Electric Stimulation, Vagus nerve, Disease Models, Animal, Oxidative Stress, Atropine, Endocrinology, chemistry, Heart failure, Nitric Oxide Synthase, Reactive Oxygen Species, Cardiology and Cardiovascular Medicine, business, Oxidation-Reduction, Acetylcholine, Oxidative stress, medicine.drug
الوصف: 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 ω-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.
تدمد: 1755-3245
0008-6363
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c73811e792becfe411a80325bb422270Test
https://doi.org/10.1093/cvr/cvm092Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....c73811e792becfe411a80325bb422270
قاعدة البيانات: OpenAIRE
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