Abstract:
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 ∑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-κB 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-κB signaling may contribute to these effects.
journal_name
Int J Cardioljournal_title
International journal of cardiologyauthors
Yu L,Meng G,Huang B,Zhou X,Stavrakis S,Wang M,Li X,Zhou L,Wang Y,Wang M,Wang Z,Deng J,Po SS,Jiang Hdoi
10.1016/j.ijcard.2017.11.071subject
Has Abstractpub_date
2018-03-15 00:00:00pages
92-98eissn
0167-5273issn
1874-1754pii
S0167-5273(17)34008-1journal_volume
255pub_type
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journal_title:International journal of cardiology
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