Kalimo H, Smith M L
Acta Neurochir Suppl (Wien). 1986;36:129-32. doi: 10.1007/978-3-7091-8859-0_35.
The structural changes during cerebal ischemia are reviewed. In the acute phase the neurons may show either pale or dark type of ischemic injury. The former is usually associated with complete ischemia and the structural alterations are fairly inconspicious, while the latter is seen in incomplete ischemia or ischemia with recirculation and is characterized by shrinkage of neurons with extensive mitochondrial swelling and astrocytic edema. Both types of injury may be irreversible, but long post-ischemic period is usually necessary to see the final outcome of the insult, all the more since the neurons may not die until after a free postischemic interval (even with resumed function) of several hours to days. The delayed death is preceded by peculiar proliferation of cytoplasmic membranes before the doomed neurons become shrunken and disintegrate. This "maturation phenomenon" or "delayed neuronal death" is understandably important since it suggests that a longer postischemic interval for therapeutic interventions may exist. Several factors both during and after the ischemic insult can modify the changes and affect the severity of the damager among the most important ones are the degree of lactic acidosis during the ischemic period, as well as the characteristics of the neurons, since excitoxic damage by transmitter substances released by the ischemic insult has been suggested to be responsible for the delayed neuronal death.
本文综述了脑缺血期间的结构变化。在急性期，神经元可能表现为苍白型或深色型缺血性损伤。前者通常与完全缺血相关，结构改变相当不明显，而后者见于不完全缺血或再灌注缺血，其特征是神经元萎缩，伴有广泛的线粒体肿胀和星形胶质细胞水肿。这两种类型的损伤都可能是不可逆的，但通常需要较长的缺血后期才能看到损伤的最终结果，尤其是因为神经元可能直到经历数小时至数天的自由缺血后间隔（即使功能恢复）才会死亡。在注定死亡的神经元萎缩和解体之前，延迟死亡之前会出现细胞质膜的特殊增殖。这种“成熟现象”或“延迟性神经元死亡”显然很重要，因为它表明可能存在更长的缺血后间隔用于治疗干预。缺血损伤期间和之后的几个因素可以改变这些变化并影响损伤的严重程度，其中最重要的是缺血期间乳酸酸中毒的程度，以及神经元的特性，因为缺血损伤释放的递质物质引起的兴奋毒性损伤被认为是延迟性神经元死亡的原因。
