Sommer Clemens
Department of Neuropathology, Johannes Gutenberg University Mainz Medical Center, Mainz, Germany.
J Neuropathol Exp Neurol. 2008 Feb;67(2):85-92. doi: 10.1097/nen.0b013e3181630ba6.
Ischemic brain damage can be prevented or at least significantly reduced when there is a preceding brief ischemic period that does not exceed the threshold for tissue damage--a phenomenon termed "ischemic preconditioning" (ischemic PC). Experimental PC in rodents is now considered to be a model for transient ischemic attacks in humans, and there is increasing hope for translating the knowledge of underlying mechanisms in the animal models into the clinic to enhance endogenous neuroprotective mechanisms in patients with stroke. However, although PC was originally defined as a subtoxic stimulus without any morphologic damage, there is a growing body of evidence from studies using sensitive techniques that postischemic structural alterations of brain tissue manifest not only after ischemia with prior PC but also after the PC stimulus itself. Furthermore, it has become evident over time that the primary shortcomings of many experimental studies on PC are the short observation intervals. The few studies with extended postischemic survival periods done to date provide clear evidence of considerable structural changes and even cell death, which may only be postponed by PC. Therefore, further studies are needed to elucidate structural long-term changes after PC and to validate the persistence of the neuroprotective effects.
当存在一个不超过组织损伤阈值的短暂缺血前期时，缺血性脑损伤是可以预防的，或者至少可以显著减轻——这种现象被称为“缺血预处理”（ischemic PC）。现在认为啮齿动物的实验性预处理是人类短暂性脑缺血发作的一个模型，并且越来越希望将动物模型中潜在机制的知识转化到临床，以增强中风患者的内源性神经保护机制。然而，尽管预处理最初被定义为一种无任何形态学损伤的亚毒性刺激，但越来越多使用敏感技术的研究证据表明，脑组织的缺血后结构改变不仅在有预处理的缺血后出现，而且在预处理刺激本身之后也会出现。此外，随着时间的推移，很明显许多关于预处理的实验研究的主要缺点是观察间隔时间短。迄今为止进行的少数延长缺血后生存期的研究提供了明确的证据，表明存在相当大的结构变化甚至细胞死亡，而这可能只是被预处理推迟了。因此，需要进一步研究以阐明预处理后的长期结构变化，并验证神经保护作用的持续性。
