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Background  With chronic ischemia after myocardial infarction, the resulting scar tissue result in electrical and structural remodeling vulnerable to an arrhythmogenic substrate. The cholinergic anti‐inflammatory pathway elicited by vagal nerve via α7 nicotinic acetylcholine receptors (α7‐n AC hR) can modulate local and systemic inflammatory responses. Here, we aimed to clarify a novel mechanism for the antiarrhythmogenic properties of vagal nerve during the ischemic cardiomyopathy ( ICM ).    Methods and Results  Left anterior descending artery of adult male Sprague‐Dawley rats was ligated for 4 weeks to develop  ICM . Western blot revealed that eliciting the cholinergic anti‐inflammatory pathway by nicotine treatment showed a significant reduction in the amounts of collagens, cytokines, and other inflammatory mediators in the left ventricular infarcted border zone via inhibited  NF ‐ κB  activation, whereas it increased the phosphorylated connexin 43. Vagotomy inhibited the anti‐inflammatory, anti‐fibrosis, and anti‐arrhythmogenic effect of nicotine administration. And immunohistochemistry confirmed that the nicotine administration‐induced increase of connexin 43 was located in intercellular junctions. Furthermore nicotine treatment suppressed  NF ‐κB activation in lipopolysaccharide‐stimulated  RAW 264.7 cells, and α‐bungarotoxin (an α7‐n AC hR selective antagonist) partly inhibited the nicotine‐treatment effect. In addition, 4‐week nicotine administration slightly improved the cardiac function, increased cardiac parasympathetic tone, decreased the prolonged  QT c, and decreased the arrhythmia score of programmed electric stimulation‐induced ventricular arrhythmia.    Conclusions  Eliciting the cholinergic anti‐inflammatory pathway exerts anti‐arrhythmogenic effects against  ICM ‐induced ventricular arrhythmia accompanied by downregulation of cytokines, downgenerating of collagens, decrease in sympathetic/parasympathetic ratio, and prevention of the loss of phosphorylated connexin 43 during  ICM . Our findings may suggest a promising therapy for the generation of  ICM ‐induced ventricular arrhythmia by eliciting the cholinergic anti‐inflammatory pathway.

Alteration of Cholinergic Anti‐Inflammatory Pathway in Rat With Ischemic Cardiomyopathy–Modified Electrophysiological Function of Heart