交感神经系统过度激活在心肌梗死后恶性室性心律失常中起重要作用，然而其机制尚不清楚。据我们已有工作基础,我们提出心肾交感神经环路重构可能是心肌梗死后交感神经系统过度激活的中心环节。我们最近研究发现无创迷走神经刺激可改善心肌梗死后的恶性室性心律失常的基质以及发生机制,故提出无创迷走神经刺激可能成为安全、有效的防治心肌梗死后恶性室性心律失常及心脏猝死的新策略。本项目拟在大型动物心肌梗死模型中从神经形态学、神经功能学方面验证心肾交感神经环路的构成。并结合在体植入式神经活性记录及神经示踪技术分析心肌梗死后心肾交感神经环路在不同时段的重构特点及其分子生物学机制。我们还将研究无创迷走神经刺激防治心肌梗死后恶性室性心律失常及心肾环路重构的最佳负荷剂量。我们的研究成果有望为深入理解心肌梗死后恶性室性心律失常的发病机制,探索新的防治手段提供科学依据。

The exaggerated sympathetic activation is a hallmark of post-infarction malignant ventricular arrhythmia, is a critical factor in the initiation and progression of post-infarction arrhythmic state. The mechanism(s) by which sympathetic excitation occurs in the post-infarction arrhythmic state are not completely understood. Our previous studies have shown that the positive feedback cardiac-renal circuit may be a crucial element of sympathetic activation. Furthermore, previous studies from our group have shown that noninvasive vagal stimulation may improve post-infarction cardiac remodeling and sympathetic neural remodeling. Therefore, we hypothesized that noninvasive vagal nerve stimulation may be an effective and safety approach for post-infarction malignant ventricular arrhythmias and sudden cardiac death . In the present project, we will investigate the roles of cardiac-renal circuit remodeling and modulation with noninvasive vagal stimulation in post-infarction ventricular arrhythmia by neural functional and morphological technique. It would provide profound theoretical basis for better understanding the mechanism and exploring an effective approach in malignant ventricular arrhythmias prevention and treatment.