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。 遭受心脏骤停脑缺血(CACI)。诱发了SD 通过在暴露的顶脑硬脑膜上应用氯化钾 大脑皮层或三天后通过海马区KCl灌流， 动物接受CACI。关于单侧海马区 KCl2灌流可诱导SD的发生。 同侧海马区，伴有明显的谷氨酸升高。 在用KCl替代的大鼠中，没有观察到这样的影响 用生理盐水溶液。海马型氯化钾动物模型 3天后接受CACI的灌流显示出显著的保护作用 灌注区一侧的CA1区锥体神经元。没有这样的效果 在Krebs-Ringer灌流的大鼠中观察到。氯化钾的保护作用 在CA1锥体神经元上，皮质也有明显的变化 应用，尽管影响更多的是双边的。SD诱发3 CACI的前几天导致显著降低了对 大鼠心脏骤停24小时后对听源性惊厥(AuSz)的反应 侮辱。 为了阐明SD的保护性质，将脑组织 在诱发SD后的不同时间间隔的速率研究 以及在各种相关的控制条件下。我们的研究表明 显著刺激同侧大脑半球蛋白质合成 至SD，仅在SD诱导3天的动物中表现出来 早些时候。在处死大鼠中，蛋白质合成酶的升高是缺失的 SD诱导后1天或7天及各对照组大鼠。

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. To elucidate the protective nature of the SD, the brain tissue was studied in rate at various time intervals following induction of the SD and in various relevant control conditions. Our studies indicated a striking stimulation of protein synthesis in the hemisphere ipsilateral to SD, which was demonstrable only in animals with SD induction 3 days earlier. Elevation of protein sysntheis was absent in rats sacrificed 1 or 7 days after SD induction and in all control groups of rats.