Journal of cardiovascular electrophysiology · 2015
Acetylcholine Suppresses Ventricular Arrhythmias and Improves Conduction and Connexin-43 Properties During Myocardial Ischemia in Isolated Rabbit Hearts.
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Aiba Takeshi, Noda Takashi, Hidaka Ichiro, Inagaki Masashi, Katare Rajesh G, Ando Motonori, Sunagawa Kenji, Sato Takayuki, Sugimachi Masaru
Аннотация
INTRODUCTION: 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-apoptotic cascades. However, electrophysiological mechanisms of the antiarrhythmic effect of ACh after acute MI are still unclear.
METHODS: Acute MI was induced by ligation of the left anterior descending (LAD) coronary artery in Langendorff-perfused rabbit hearts with (ACh(+):n = 11) or without (ACh(-):n = 12) 10 μmol/L ACh delivered continuously starting at 5 minutes before LAD ligation. Action potentials on the left ventricular (LV) anterior surface (≈2×2 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-43 was analyzed by immunoblotting and immunohistochemistry.
RESULTS: Averaged CV in the ischemic border zone (IBZ) was significantly slower in ACh(-) than in ACh(+) (21 ± 7 vs. 34 ± 6 cm/s; P < 0.01). Short-coupled extra stimulus further decreased CV of IBZ in ACh(-) (13 ± 4 cm/s) but did not change that in ACh(+) (34 ± 5 cm/s), leading to a high incidence of conduction block in IBZ in ACh(-) but not in ACh(+) (83% vs. 0%). VT/VF after MI were induced in ACh(-) but suppressed in ACh(+) (10/12 vs. 3/11; P < 0.01). Connexin-43 in the LV anterior wall was significantly reduced after MI in ACh(-) but not in ACh(+).
CONCLUSION: ACh may suppress VT/VF by preventing loss of Gj and improving CV in IBZ during acute MI.
METHODS: Acute MI was induced by ligation of the left anterior descending (LAD) coronary artery in Langendorff-perfused rabbit hearts with (ACh(+):n = 11) or without (ACh(-):n = 12) 10 μmol/L ACh delivered continuously starting at 5 minutes before LAD ligation. Action potentials on the left ventricular (LV) anterior surface (≈2×2 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-43 was analyzed by immunoblotting and immunohistochemistry.
RESULTS: Averaged CV in the ischemic border zone (IBZ) was significantly slower in ACh(-) than in ACh(+) (21 ± 7 vs. 34 ± 6 cm/s; P < 0.01). Short-coupled extra stimulus further decreased CV of IBZ in ACh(-) (13 ± 4 cm/s) but did not change that in ACh(+) (34 ± 5 cm/s), leading to a high incidence of conduction block in IBZ in ACh(-) but not in ACh(+) (83% vs. 0%). VT/VF after MI were induced in ACh(-) but suppressed in ACh(+) (10/12 vs. 3/11; P < 0.01). Connexin-43 in the LV anterior wall was significantly reduced after MI in ACh(-) but not in ACh(+).
CONCLUSION: ACh may suppress VT/VF by preventing loss of Gj and improving CV in IBZ during acute MI.