急性心肌梗死(AMI) 是世界上致死和致残的主要病因。及时再灌注法是AMI的标准疗法，能够缩小梗死面积，提高患者存活率和改善预后。然而，25 %的患者在患心肌梗死(Ml) 后会进一步发展成为心力衰竭(HF)，且其中50%的患者会在5年内死亡。由于梗死面积是预断病人病情( 包括HF的形成) 的主要指标，因此，改善心肌的治疗方法具有极大的应用前景。 在过去30年中，研究者已发现多种能够刺激内源性心肌保护通道的刺激物，这些刺激物能在缺血预适应(IPC)和缺血后适应以及心肌缺血情况下启动保护机制。当在心肌缺血发生前、发生期间或发生后即刻使用刺激物，在远离心脏的血管床中发生的短暂、可逆性局部缺血就会即刻引发心肌保护机制——这种现象被分别称为远程缺血预适应，远程缺血期适应和远程缺血后适应。尽管目前的研究尚未完全阐明远程缺血预适应(RIPC) 的作用机制，但RIPC与IPC在机制上有很多共同之处。RIPC的发现使研究转向了远程非缺血刺激的应用，包括神经刺激( 脊髓刺激和迷走神经刺激) 以及电针(EA)。笔者与其他研究人员发现并阐述了非缺血现象的机制，并将其定义为远程创伤预适 应(RPCT)。通过刺激皮肤感觉神经来启动RPCT，这与穴位处神经刺激和EA既有相似性又有一定差异性。笔者在此次研究中还发现，可通过采用腹中线电刺激(与EA疗法相似) 来模拟RPCT，而且作为预适应刺激和后适应刺激( 在应用再灌注法时)，这种激活心肌保护机制的模式是非常有效的。通过对这些心肌保护现象的研究，学术界对心肌保护机制形成了一种全面且综 合的理解，而且在过去的5~10 年期间, 这种理解变得逐渐清晰，即无论是缺血性刺激诱导还是非缺血性刺激诱导，其机制均相似。通过对文献中多种数据的综合考虑，我们认为所有的这些心肌保护'适应'现象均表示心肌保护机制的启动是从心肌适 应网(含有特定介质和心肌细胞生存感受器) 的不同切入点进行的，该切入点包括NF-κB、Stat3/5、蛋白激酶C、舒缓激肽和mitoK_ATP 通道。神经系统传导通路可能代表了一种激活心脏和其他器官适应的新机制。研究表明，由于IPC和RIPC存在一定风险并且无法应用于某些患者，所以它们很难被转化为临床应用。因此，近期又新兴了一种神经刺激和痛感刺激的应用，这是一种激活心肌适应的潜在的非缺血性无创方法。作为引起心脏保护作用众多方法之一的后适应重点强调了临床相关性，这种临床相关性有助于在现有成熟的药物与电子疗法中加速新的治疗方向的突破。

Acute myocardial infarction (AMI) is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. However, 25% of patients proceed to develop heart failure (HF) after myocardial infarction (MI) and 50% of these will die within five years. Since the size of the infarct is the major predictor of the outcome, including the development of HF, therapies to improve myocardial salvage have great potential. Over the past three decades, a number of stimuli have been discovered that activate endogenous cardioprotective pathways. In ischemic preconditioning (IPC) and ischemic postconditioning, ischemia within the heart initiates the protection. Brief reversible episodes of ischemia in vascular beds remote from the heart can also trigger cardioprotection when applied before, during, or immediately after myocardial ischemia—known as remote ischemic pre-, per-, and post-conditioning, respectively. Although the mechanism of remote ischemic preconditioning (RIPC) has not yet been fully elucidated, many mechanistic components are shared with IPC. The discovery of RIPC led to research into the use of remote non-ischemic stimuli including nerve stimulation (spinal and vagal), and electroacupuncture (EA). We discovered and, with others, have elucidated mechanistic aspects of a non-ischemic phenomenon we termed remote preconditioning of trauma (RPCT). RPCT operates via neural stimulation of skin sensory nerves and has similarities and differences to nerve stimulation and EA conducted at acupoints. We show herein that RPCT can be mimicked using electrical stimulation of the abdominal midline (EA-like treatment) and that this modality of activating cardioprotection is powerful as both a preconditioning and a postconditioning stimulus (when applied at reperfusion). Investigations of these cardioprotective phenomena have led to a more integrative understanding of mechanisms related to cardioprotection, and in the last five to ten years, it has become clear that the mechanisms are similar, whether induced by ischemic or non-ischemic stimuli. Taking together much of the data in the literature, we propose that all of these cardioprotective 'conditioning' phenomena represent activation from different entry points of a cardiac conditioning network that converges upon specific mediators and effectors of myocardial cell survival, including NF-кB, Stat3/5, protein kinase C, bradykinin, and the mitoK_ATP channel. Nervous system pathways may represent a novel mechanism for initiating conditioning of the heart and other organs. IPC and RIPC have proven difficult to translate clinically, as they have associated risks and cannot be used in some patients. Because of this, the use of neural and nociceptive stimuli is emerging as a potential non-ischemic and non-traumatic means to initiate cardiac conditioning. Clinical relevance is underscored by the demonstration of postconditioning with one of these modalities, supporting the conclusion that the development of pharmaceuticals and electroceuticals for this purpose is an area ripe for clinical development.