心肌缺血诱导心脏感觉神经上的辣椒素受体（TRPV1）活化将伤害感受信号传至脊髓，已知预处理介导的TRPV1活化可减轻心肌缺血再灌注损伤（IRI），但其过度活化也可能加重心肌损伤，其机制尚待阐明；心肌缺血后神经生长因子（NGF）表达增加，其可致敏TRPV1，NGF-TRPV1敏化在心肌IRI中发挥何种作用，仍不清楚。我们前期研究发现中枢远端阿片预处理（ROPC）通过激活脊髓阿片受体减轻心肌IRI，鉴于阿片类可抑制TRPV1或NGF信号，我们推测：鞘内ROPC可能通过抑制脊髓NGF-TRPV1敏化发挥心肌保护作用。本课题利用9.4T MRI扫描心肌缺血后脊髓神经信号，并应用RNA干扰、膜片钳等方法，研究鞘内ROPC对心肌缺血后脊髓NGF-TRPV1敏化及伤害感受信号传导的影响，并探讨其调控NGF-TRPV1敏化的机制。本课题将阐明ROPC发挥心肌保护作用的神经信号机制，为其临床应用提供依据。

The vanilloid receptor (TRPV1) distributed on the cardiac sensory nerve is activated by cardiac ischemia, transmitting the nociceptive signal from heart to spinal cord. It is known that preconditioning induced TRPV1 activation could reduce myocardial ischemia reperfusion injury (IRI), while its overactivation may also exacerbate myocardial injury. Nerve growth factor (NGF) was reported upregulated after cardiac ischemia, which in turn resulted in TRPV1 sensitization. However, it is unclear whether NGF-induced TRPV1 sensitization contributes to myocardial IRI. We had demonstrated that central remote opioid preconditioning(ROPC) reduced myocardial IRI in rat via activating the three opioid receptors in spinal cord. In view of that opioids could negatively regulate TRPV1 or NGF signaling, we therefore presume that intrathecal ROPC might exert cardioprotective effects via inhibiting spinal NGF-TRPV1 sensitization. This study proposes to investigate the effects of intrathecal ROPC on spinal NGF-TRPV1 sensitization and subsequent nociceptive signal transduction following cardiac ischemia, as well as the molecular mechanism of ROPC regulating NGF-TRPV1 sensitization. The neuronal activity in spine cord following cardiac ischemic will be detected by using 9.4T high field MRI system; In addition, shRNA interference, whole cell patch clamp and other molecular biological techniques will also be used in the experiments. This study will clarify the neuronal signaling mechanisms of ROPC exerting cardioprotective effects, and provide a theoretical basis for its clinical application.