期刊
INTERNATIONAL JOURNAL OF CARDIOLOGY
卷 255, 期 -, 页码 92-98出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.ijcard.2017.11.071
关键词
Gut microbes; Trimethylamine N-oxide; Autonomic nervous system; Atrial fibrillation; Inflammation
资金
- National Natural Science Foundation of China [81530011, 81570463, 81600395, 81270339, 81300182]
- Natural Science Foundation of Hubei Province [2016CFA065, 2016CFA048, 2016CFB621]
Background: Emerging evidence indicates gut microbes and their products could activate the autonomic nervous system (ANS), which plays important roles in the initiation and maintenance of atrial fibrillation (AF). Trimethylamine N-oxide (TMAO), a metabolite derived from gut microbes, is associated with cardiovascular diseases. The present study aimed to investigate the role of TMAO in the progression of AF. Methods: In part 1: TMAO or saline was locally injected into 4 major atrial ganglionated plexi (GP) to clarify its effect on cardiac ANS and AF inducibility in normal canines. In part 2: TMAO or saline was injected into 4 major atrial GP to test its effect on AF progression in a rapid atrial pacing (RAP)-induced AF model. Results: In part 1: Local injection of TMAO significantly increased anterior right GP (ARGP) function and neural activity, shortened ERP values. In part 2, compared with the control group, 6-hour RAP significantly shortened the ERP, widened the Sigma WOV, enhanced the ARGP function and neural activity, increased the NGF and c-fos expression, and up-regulated the inflammatory cytokines. TMAO aggravated all of these changes by activating the proinflammatory p65 NF-kappa B signaling pathway. Conclusions: TMAO could increase the instability of atrial electrophysiology in normal canines and aggravate the acute electrical remodeling in a RAP-induced AF model by exacerbating autonomic remodeling. The increased inflammatory cytokines in the GP due to the activation of p65 NF-kappa B signaling may contribute to these effects. (c) 2017 Elsevier B.V. All rights reserved.
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