针灸治疗缺血性心脏病疗效确切。我们前期研究表明，针刺心经可通过海马调控自主神经系统，从而改善心肌缺血。神经科学研究提示，蓝斑核、内侧隔核、海马是边缘系统中一些重要的内脏调节核团，起源于蓝斑的去甲肾上腺素能和起源于内侧隔核的胆碱能神经元共同组成神经通路直接投射到海马。本项目组明确提出针刺抗心肌缺血效应可能是通过蓝斑核/内侧隔核-海马通路调节海马功能，继而实现对自主神经系统的调控。以电针干预急性心肌缺血作用的中枢神经调控机制为切入点，通过复制大鼠急性心肌缺血模型，运用电生理、免疫组化、在线微透析、光遗传学等技术，观察心电图和血流动力学指标，蓝斑核、内侧隔核、海马神经元放电和fos 蛋白及c-fos基因表达，以及蓝斑核、内侧隔核神经递质含量等，探讨蓝斑核/内侧隔核-海马通路在针刺抗心肌缺血效应中的作用，并进一步明确上述神经通路神经元的性质，从而揭示针刺心经改善急性心肌缺血作用的中枢调控机制。

Acupuncture has an obvious effect on the treatment of ischemic heart diseases. Our previous studies have demonstrated that acupuncture at the heart channel of hand-shaoyin (HT) could improve myocardial ischemia by regulating and controlling autonomic nervous system through hippocampus. Neuro-scientific research suggests that locus coeruleus (LC), medial septal nucleus (MS) and hippocampus are very significant visceral regulating nucleuses in the limbic system. The norepinephrine neurons and the cholinergic neurons are respectively originated from LC and MS that co-form the neural pathway to directly project to the hippocampus. Accordingly, we further propose that the effects of acupuncture at HT on the treatment of myocardial ischemia could adjust the hippocampal function, then regulate the autonomic nervous system through the LC/MS-hippocampus pathways. .The current research will start with the central nervous regulating mechanism of electro-acupuncture at HT in the treatment of acute myocardial ischemia by duplicating acute myocardial ischemia model in rats. We will employ experimental technologies, such as electrophysiology, immunohistochemistry, on-line microdialysis, and optogenetics to observe the ECG and hemodynamic index, the neurons discharge, fos protein and c-fos gene expression of LC, MS and hippocampus, and the neurotransmitter contents of LC and MS. We will discuss the function of acupuncture at HT in the treatment of myocardial ischemia through the LC-hippocampus and MS-hippocampus pathways, and further clarify the property of two neural pathways in order to reveal the function of acupuncture at HT in central regulatory mechanism to improve acute myocardial ischemia.