ROLE OF SPREADING DEPRESSION IN CARDIAC ARREST CEREBRAL ISCHEMIA

在大鼠中研究了扩散性抑制（SD）的作用 心脏骤停脑缺血（CACI）。 诱导SD 通过在暴露的顶叶大脑硬脑膜上应用KCl 皮质或通过KCl灌注通过海马。 三天后 动物进行CACI。 关于海马体单侧 定期灌注KCl导致SD的诱导， 同侧海马，与谷氨酸显著升高相关。 在用KCl替代KCl的大鼠中没有观察到这种效应。 生理盐水 海马KCl灌注动物， 3天后给予CACI，显示出显著的保护CA 1 在灌注侧的锥体神经元。 没有这样的效果， 在Krebs-Ringer灌注大鼠中观察到。KCl对细胞的保护作用 CA 1锥体神经元在皮层应用后也很明显， 尽管影响是双向的。 CACI前3天诱导SD 导致大鼠对听觉源性的敏感性显著降低， 在心脏骤停损伤后24小时测试时，

The role of the spreading depression (SD) was investigated in rats subjected to cardiac arrest cerebral ischemia (CACI). The SD was induced by application of KCl either on the exposed dura of the parietal cerebral cortex or by KCl perfusion through the hippocampus. Three days later, the animals underwent the CACI. With regard to the hippocampus unilateral perfusion with KCl regularly resulted in induction of the SD in the ipsilateral hippocampus, associated with marked elevation of glutamate. No such effect was observed in rats in which KCl had been substituted with physiologic saline solution. Animals with hippocampal KCl perfusion, followed 3 days later by CACI, showed significant protection of CA1 pyramidal neurons on the side of the perfusion. No such effect was observed in Krebs-Ringer perfused rats. The protective effect of KCl on CA1 pyramidal neurons was evident also following the cortical application, although the effect was more bilateral. The SD induced 3 days before CACI resulted in a marked reduction in the susceptibility of rats to audiogenic seizures (AuSz) when tested 24 hr after cardiac arrest insult.