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Background: In recent years, as the coronary thrombolysis, promotion and use of percutaneous transluminal coronary angioplasty (percutaneous transluminal coronary angioplasty, PCTA), coronary artery bypass graft surgery (coronary artery bypass grafting, CABG), myocardial The reperfusion injury widespread attention. Reperfusion injury usually presents reperfusion arrhythmias. Gap junctions (gap junction, GJ) uncoupling of the myocardial the electrical conduction slowing and the repolarization inconsistent closely related. Acidosis, ischemia-reperfusion induced calcium overload and lipid metabolite accumulation is a decisive factor in cell GJ uncoupling. Antiarrhythmic peptide (antiarrhythmic peptide 10, AAP10) is an the GJ agonist, on the role of AAP10 on ischemia-reperfusion arrhythmias little. Objective: To observe GJ agonist antiarrhythmic peptide (AAP10) on myocardial ischemia reperfusion arrhythmias, and to explore its mechanism. Methods: 40 Japanese white rabbits were randomly divided into ischemia-reperfusion (ischemia reperfusion, IR) group, AAP10 low concentration group, the concentration of groups in AAP10, AAP10 high concentration group, 10 in each group. Preparation of rabbit left ventricular wedge myocardial reperfusion model block. Perfused normal Tyrode solution stability after ischemia-reperfusion group stopping irrigation 40min reperfusion. AAP10 group perfused normal Tyrode's solution is low, medium and high concentrations AAP10 (100nmol / L, 500nmol / L, 1000nmol / L) stable stopping irrigation after 40 min reperfusion. (Stimulus response between perfusion throughout the same time using floating glass microelectrodes synchronization record subendocardial, subepicardial myocardial transmembrane action potential across the wall of the ECG (electrocardiogram, ECG), and the observation of epicardial myocardial stimulation interval, SRI), the rate of ventricular tachycardia (ventricular arrhythmias, VT)-induced and ischemia-reperfusion myocardial recovery time. After the end of the experiment, measurement of left ventricular wedge myocardial block weight, left ventricular weight, heart weight. Results: ① left ventricular wedge myocardial block weight and LVW than heart weight was no significant difference (P> 0.05); ② ischemia-reperfusion group, AAP10 low, medium, and high concentrations of ventricular cardiac over The speed incidence was 100% (10/10), 50% (5/10) 20% (2/10) and 1% (1/10) (P <0.05); ③ in different concentrations of AAP10 group, SRI compared with the IR group were significantly reduced (P <0.01); ④ different AAP10 concentration group after ischemia-reperfusion myocardial recovery time was significantly shorter (P <0.01) than those in the IR group; ⑤ in AAP10 group before and after treatment the heart film and epicardial action potential morphology and time were no significant changes (P> 0.05). Conclusion: ① myocardial ischemia-reperfusion injury, significantly increased the incidence of arrhythmia caused by reperfusion. Which may be related GJ uncoupling induced myocardial electrical conduction slowing repolarization related to inconsistent; ② The AAP10 can shorten myocardial stimulation of the reaction period, thus speeding up the conduction shortened myocardial recovery time, protect the damaged myocardium reduce reperfusion cardiac rhythm The incidence of disorders, its mechanism may improve GJ coupling state; ③ AAP10 not affect the action potential morphology and time, so no arrhythmogenic effect GJ agonist is expected to become a new hot spot for the treatment of cardiac arrhythmias.
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