急性心梗时交感神经过度活动以及陈旧性心梗时心脏交感神经再生、重塑及异常活动在缺血性心律失常和心源性猝死发生中起关键性触发作用。降低交感神经的传出活动及其效应对防治心源性猝死有重要价值，相应手段包括“突触前”策略（包括抑制交感神经递质释放和促进递质去甲肾上腺素（NE）回摄取）和“突触后”策略（拮抗肾上腺素受体或其它交感神经伴随递质受体）。本项目拟探讨一种突触前措施，即选择性敲低（knockdown）交感神经中与递质囊泡胞吐关系密切的突触结合蛋白I （synaptotagmin I，SYT1）来抑制递质NE释放，以期取消心律失常的触发因素，观察这种措施是否可降低心梗后致命性心律失常的发生率。预期结果将给冠心病/心源性猝死的防治提供一种新策略。

Cardiac sympathetic nerve overactivity and remodeling during acute, healing and healed myocardial infarction (MI) play a key triggering role in the occurrence of ischemic arrhythmias and sudden cardiac death (SCD). Suppressing sympathetic output and its effects has important value in the prevention and treatment for ishchemic arrhythmias and SCD, and the corresponding means include “presynaptic” strategies (i.e., reducing sympathetic neurotransmitter release and increasing norepinephrine reuptake) and "postsynaptic" strategies (such as antagonizing adrenoceptors or other receptors of sympathetic co-transmitters). This project aimed to specifically knockdown synaptotagmin I (SYT1）in rat sympathetic nerves, a protein involved in the exocytosis of synaptic vesicles, to decrease sympathetic neurotransmitter release and thus to abolish the trigger of arrhythmias, and further to observe if this strategy could reduce the occurrence of post-MI lethal arrhythmias and SCD.