室性心律失常是心肌梗死(MI)后心脏性猝死的主要原因，而交感神经活性增高是MI慢性期室性心律失常发生的主要机制。我们前期的研究发现，肾脏去交感神经术（RSD）在MI慢性期可阻断持续性交感神经系统及RAAS系统的激活，进而延缓或逆转左心室重构。研究表明，RSD抑制交感神经活性具有潜在的治疗室性心律失常作用，但具体机制不明。本课题拟采用犬MI慢性期室性心律失常模型，分别给予RSD治疗、假RSD术和美托洛尔药物干预，比较干预前后，各组犬心电生理，心功能，交感神经形态、神经递质释放、神经放电、神经重构、神经分子，心肌细胞离子通道电流和通道分子表达的动态变化，阐明RSD防治MI慢性期室性心律失常的效果及机制。明确RSD防治MI慢性期室性心律失常的可行性，为MI慢性期室性心律失常治疗提供新的思路和理论依据。

It is known that ventricular arrythmias is a major cause of sudden cardiac deaths. Sympathetic neural activation abnormality is the main mechanism for the occurrence of ventricular arrhythmias which is the frequent complication of myocardial infarction (MI).Number of studies done by us showed that renal sympathetic denervation (RSD) can treat arrhythmia by blocking the sympathetic nervous and RAAS activity,reverse the remoleding of left ventricular ,but the exact mechanism of how RSD affect the sympathetic activity remains unclear. Based on what has been mentioned above,we hypothesis that RSD could modify cardiac sympathetic nerve activity, reverse sympathetic neural remodeling, reduce the occurrence of ventricular arrythmia after MI. Canine models with MI are introduced after ligating the proximal left coronary artery, the dogs were randomly allocated to undergo RSD, sham RSD and metoprolo treatment respectively. By comparing the electrophysology characteristic and ionic channel cheanges ,the sympathetic activation and remodeling changes ,the nerve growth factor morphology and the transformation of mRNA expression in different groups after MI,We formulate that the exact neurohormonal and molecular mechanism of how RSD affects the sympathetic nerve activity, thus provide the theoretical foundation for the treatment of ventricular arrhythmias which is generated by MI.