Sommer Clemens
Department of Neuropathology, Mainz University Medical Center, Langenbeckstrasse 1, 55131, Mainz, Germany.
Acta Neuropathol. 2009 May;117(5):511-23. doi: 10.1007/s00401-008-0473-0. Epub 2008 Dec 16.
Transient ischemic attacks (TIAs) have recently become the center of attention since they are thought to share some characteristics with experimental ischemic preconditioning (IPC). This phenomenon describes the situation that a brief, per se harmless, cerebral ischemic period renders the brain resistant to a subsequent severe and normally damaging ischemia. Preconditioning (PC) is not restricted to the brain but also occurs in other organs. Furthermore, apart from a short ischemia, the PC event may comprise nearly any noxious stimulus which, however, must not exceed the threshold to tissue damage. In the last two decades, our knowledge concerning the underlying molecular basis of PC has substantially grown and there is hope to potentially imitate the induction of an endogenous neuroprotective state in patients with a high risk of cerebral ischemia. While, at present, there is virtually no neuropathological data on changes after TIAs or TIA-like PC ischemic periods in human brains, the following review will briefly summarize the current knowledge of plastic neuronal changes after PC in animal models, still awaiting their detection in the human brain.
短暂性脑缺血发作（TIAs）近来已成为关注焦点，因为它们被认为与实验性缺血预处理（IPC）具有某些共同特征。这种现象描述的是，一段短暂的、本身无害的脑缺血期会使大脑对随后严重的、通常具有破坏性的缺血产生耐受性。预处理（PC）并不局限于大脑，在其他器官中也会发生。此外，除了短暂缺血外，PC事件可能包括几乎任何有害刺激，但该刺激不得超过组织损伤阈值。在过去二十年中，我们关于PC潜在分子基础的知识有了显著增长，并且有望在具有高脑缺血风险的患者中潜在地模拟内源性神经保护状态的诱导。虽然目前几乎没有关于人类大脑中TIAs或类似TIA的PC缺血期后变化的神经病理学数据，但以下综述将简要总结动物模型中PC后可塑性神经元变化的当前知识，仍有待在人类大脑中进行检测。
