Sublethal hypoxic or ischemic events can improve the tolerance of tissues, organs, and even organisms from subsequent lethal injury caused by hypoxia or ischemia. This phenomenon has been termed hypoxic or ischemic preconditioning (HPC or IPC) and is well established in the heart and the brain. This review aims to discuss HPC and IPC with respect to their historical development and advancements in our understanding of the neurochemical basis for their neuroprotective role. Through decades of collaborative research and studies of HPC and IPC in other organ systems, our understanding of HPC and IPC-induced neuroprotection has expanded to include: early- (phosphorylation targets, transporter regulation, interfering RNA) and late- (regulation of genes like EPO, VEGF, and iNOS) phase changes, regulators of programmed cell death, members of metabolic pathways, receptor modulators, and many other novel targets. The rapid acceleration in our understanding of HPC and IPC will help facilitate transition into the clinical setting.

亚致死性缺氧或局部缺血事件可提高组织，器官乃至生物体的耐受性，使其免受缺氧或局部缺血引起的后续致死性伤害。这种现象已被称为缺氧或缺血预处理（HPC或IPC），并且在心脏和大脑中已得到很好的确立。这篇综述旨在讨论HPC和IPC的历史发展和进展，以便我们了解其神经保护作用的神经化学基础。通过数十年来在其他器官系统中对HPC和IPC的合作研究，我们对HPC和IPC诱导的神经保护的理解已扩展到包括：早期（磷酸化靶标，转运蛋白调控，干扰RNA）和后期（调控类似基因EPO，VEGF和iNOS）相变，程序性细胞死亡的调节剂，代谢途径的成员，受体调节剂和许多其他新颖的靶标。我们对HPC和IPC的了解的迅速加速将有助于促进向临床环境的过渡。