{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T14:04:05Z","timestamp":1781013845766,"version":"3.54.1"},"reference-count":48,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,6,8]],"date-time":"2015-06-08T00:00:00Z","timestamp":1433721600000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[2015,6]]},"abstract":"<jats:title>ACh Prevents Ischemic Loss of Gj and Arrhythmias<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>Acetylcholine (ACh), a vagal efferent neurotransmitter, markedly improves survival in rats with myocardial ischemia (MI) by preventing ischemic loss of gap junction (Gj) and by inducing anti\u2010apoptotic cascades. However, electrophysiological mechanisms of the antiarrhythmic effect of ACh after acute MI are still unclear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Acute MI was induced by ligation of the left anterior descending (LAD) coronary artery in Langendorff\u2010perfused rabbit hearts with (ACh(+):n = 11) or without (ACh(\u2013):n = 12) 10 \u03bcmol\/L ACh delivered continuously starting at 5 minutes before LAD ligation. Action potentials on the left ventricular (LV) anterior surface (\u22482\u00d72 cm) were recorded by optical mapping during pacing from the LV epicardium (BCL = 500 milliseconds). Conduction velocities (CVs) at 256 sites were calculated and the ventricular tachycardia\/ventricular fibrillation (VT\/VF) susceptibility was also assessed by programmed electrical stimulation before and 30 minutes after MI. The amount and distribution of Gj protein connexin\u201043 was analyzed by immunoblotting and immunohistochemistry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Averaged CV in the ischemic border zone (IBZ) was significantly slower in ACh(\u2013) than in ACh(+) (21 \u00b1 7 vs. 34 \u00b1 6 cm\/s; P &lt; 0.01). Short\u2010coupled extra stimulus further decreased CV of IBZ in ACh(\u2013) (13 \u00b1 4 cm\/s) but did not change that in ACh(+) (34 \u00b1 5 cm\/s), leading to a high incidence of conduction block in IBZ in ACh(\u2013) but not in ACh(+) (83% vs. 0%). VT\/VF after MI were induced in ACh(\u2013) but suppressed in ACh(+) (10\/12 vs. 3\/11; P &lt; 0.01). Connexin\u201043 in the LV anterior wall was significantly reduced after MI in ACh(\u2013) but not in ACh(+).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>ACh may suppress VT\/VF by preventing loss of Gj and improving CV in IBZ during acute MI.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jce.12663","type":"journal-article","created":{"date-parts":[[2015,3,17]],"date-time":"2015-03-17T07:57:44Z","timestamp":1426579064000},"page":"678-685","source":"Crossref","is-referenced-by-count":7,"title":["Acetylcholine Suppresses Ventricular Arrhythmias and Improves Conduction and Connexin\u201043 Properties During Myocardial Ischemia in Isolated Rabbit Hearts"],"prefix":"10.1111","volume":"26","author":[{"given":"TAKESHI","family":"AIBA","sequence":"first","affiliation":[{"name":"Division of Arrhythmia and Electrophysiology Department of Cardiovascular 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