{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T06:55:50Z","timestamp":1791528950580,"version":"4.3.4"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,9,22]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              With chronic ischemia after myocardial infarction, the resulting scar tissue result in electrical and structural remodeling vulnerable to an arrhythmogenic substrate. The cholinergic anti\u2010inflammatory pathway elicited by vagal nerve via \u03b17 nicotinic acetylcholine receptors (\u03b17\u2010n\n              <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n              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 (\n              <jats:styled-content style=\"fixed-case\">ICM<\/jats:styled-content>\n              ).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Left anterior descending artery of adult male Sprague\u2010Dawley rats was ligated for 4\u00a0weeks to develop\n              <jats:styled-content style=\"fixed-case\">ICM<\/jats:styled-content>\n              . Western blot revealed that eliciting the cholinergic anti\u2010inflammatory 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\n              <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\n              \u2010\n              <jats:styled-content style=\"fixed-case\">\u03baB<\/jats:styled-content>\n              activation, whereas it increased the phosphorylated connexin 43. Vagotomy inhibited the anti\u2010inflammatory, anti\u2010fibrosis, and anti\u2010arrhythmogenic effect of nicotine administration. And immunohistochemistry confirmed that the nicotine administration\u2010induced increase of connexin 43 was located in intercellular junctions. Furthermore nicotine treatment suppressed\n              <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\n              \u2010\u03baB activation in lipopolysaccharide\u2010stimulated\n              <jats:styled-content style=\"fixed-case\">RAW<\/jats:styled-content>\n              264.7 cells, and \u03b1\u2010bungarotoxin (an \u03b17\u2010n\n              <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>\n              hR selective antagonist) partly inhibited the nicotine\u2010treatment effect. In addition, 4\u2010week nicotine administration slightly improved the cardiac function, increased cardiac parasympathetic tone, decreased the prolonged\n              <jats:styled-content style=\"fixed-case\">QT<\/jats:styled-content>\n              c, and decreased the arrhythmia score of programmed electric stimulation\u2010induced ventricular arrhythmia.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              Eliciting the cholinergic anti\u2010inflammatory pathway exerts anti\u2010arrhythmogenic effects against\n              <jats:styled-content style=\"fixed-case\">ICM<\/jats:styled-content>\n              \u2010induced 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\n              <jats:styled-content style=\"fixed-case\">ICM<\/jats:styled-content>\n              . Our findings may suggest a promising therapy for the generation of\n              <jats:styled-content style=\"fixed-case\">ICM<\/jats:styled-content>\n              \u2010induced ventricular arrhythmia by eliciting the cholinergic anti\u2010inflammatory pathway.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.117.006510","type":"journal-article","created":{"date-parts":[[2017,9,20]],"date-time":"2017-09-20T01:00:24Z","timestamp":1505869224000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":31,"title":["Alteration of Cholinergic Anti\u2010Inflammatory Pathway in Rat With Ischemic Cardiomyopathy\u2013Modified Electrophysiological Function of Heart"],"prefix":"10.1161","volume":"6","author":[{"given":"Shu\u2010Jie","family":"Wu","sequence":"first","affiliation":[{"name":"Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 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