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13 April 2018 : Animal Research  

Clinical Effects of “Selective Drug” Regulating Vagus Nerve Signal Pathway in Vagally-Mediated Atrial Fibrillation

Xue Lou1BCDEFG, Yanmei Lu1BCDG, Baopeng Tang1AFG, Xianhui Zhou1AFG*

DOI: 10.12659/MSM.906044

Med Sci Monit 2018; 24: ANS2210-2217

Abstract

BACKGROUND: The cardiac autonomic nervous system plays a crucial role in genesis and development of atrial fibrillation (AF) through the G protein signal transduction pathway. Therefore, intervening in the G protein signal transduction pathway may be a new “selective drug” method to regulate autonomic nerve activity to prevent vagally-mediated AF.

MATERIAL AND METHODS: Seventeen adult beagles were randomized into 3 groups: shame-operation control group (group A, n=5), empty vector gene control group (group B, n=6), and Gαi2ctp gene experimental group (group C, n=6). Group A was injected with normal saline into the anterior atrial wall, and group B and group C animals were injected with recombinant adenovirus with empty vector or Gαi2ctp vector in the same region. AF was induced by the method of rapid atrial pacing in groups B and C. To determine the clinical effect of vagal modulation, the effective refractory periods (ERP) and field action potential duration (FAPD) were evaluated by electrophysiological study. The expression levels of tyrosine hydroxylase (TH) and choline acetyl transferase (CHAT) in different parts were determined with immunohistochemistry.

RESULTS: After successful Gai2ctp gene transfer, in group B, the ERP and FAPD significantly decreased (P<0.05), and TH and CHAT expression observably increased (P<0.05), while those differences were absent between groups A and C (P>0.05).

CONCLUSIONS: Recombinant adenovirus-mediated overexpression of Gαi2ctp in canine myocardial cells can interfere with the activity of the vagus nerve, reverse the development and progression of electrical remodeling, and reduce the incidence of AF.

Keywords: Atrial Fibrillation, Atrial Remodeling, Autonomic Nervous System, GTP-Binding Protein Regulators

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750