迷走神经是房颤发生和维持的重要机制，去迷走神经消融是房颤消融领域的热点，能明显提高房颤消融的成功率。心脏迷走神经末梢释放突触前递质乙酰胆碱，通过G-蛋白激活内向整流钾电流（IK-Ach）可诱发房颤。我们前期研究发现，左心房局部注射Gαi2 C-terminal peptide（Gαi2ctp）可以干扰迷走神经活性，减少迷走介导的房颤的发生，但以肽段为基础的药物治疗需要肽段在心房肌细胞内持续而可控的表达，故其应用受到一定程度的制约。据此，本研究拟采用快速起搏建立的犬房颤模型，构建表达Gαi2ctp基因的质粒DNA载体，通过开胸局部注射及电穿孔的方法靶向转导至犬左心房，干扰迷走神经活性，减少迷走神经介导的房颤的发生，并从电生理学、组织学、分子生物学等角度验证其疗效，明确基因靶向干预治疗的有效性及可行性，为房颤的基因治疗提供新的思路和理论依据。

The parasympathetic nervous system is known to be involved in the genesis and maintain of AF.Vagal dennervation ablation is a hotspot in the field of AF therapy, it can obviously improve the success rate of the ablation of AF. Parasympathetic signalling in the heart is initiated upon presynaptic release of acetylcholine (ACh),which activates an inward rectifying k+ current, IK-ACh through G-protein and induces the occurrence of AF.Our initial research demonstrated the feasibility of using injection of Gαi2 C-terminal peptide (Gαi2ctp) to achieve selective parasympathetic denervation in the left atrial , with a resulting decrease vagal-induced atrial fibrillaiton. However,the utility of such a peptide-based pharmacotherapy requires sustained and controlled intracellular expression of peptide in the atrial myocardium,so restricts the application by certain degree.Accordingly,in the present study, we establish the rapid pacing atrial fibrillation model of canine,construct the plasmid DNA vector expressing Gαi2ctp gene, and targeted transduction to the left atrium through the method of open-heart local injection and electroporation .The Gαi2ctp gene attenuates parasympathetic activity and reduces vagal-induced AF. And verify the feasibility from the electrophysiology, histology, molecular biology etc .To investigate the validity and feasibility of Gene targeting intervention treatment, provide new ideas and theoretical basis for gene therapy of AF .