ROLE OF SPREADING DEPRESSION IN CARDIAC ARREST CEREBRAL ISCHEMIA

抑郁扩散在心脏骤停脑缺血中的作用

• 批准号: 2579650
• 负责人: N KAWAHARA
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/2579650
• 关键词: cerebral cortex; cerebral ischemia /hypoxia; disease /disorder model; glutamates; heart arrest; hippocampus; laboratory rat; potassium chloride; protein biosynthesis; pyramidal cells; reflex epilepsy; spreading cortical depression

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.

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 皮层或通过KCl灌注海马三天后， 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KCl替代的大鼠中未观察到这种效应 用生理盐水 海马KCl动物 灌注，3天后CACI，显示出显着的保护作用， CA 1区锥体神经元的数量。 没有这样的效果 在Krebs-Ringer灌注大鼠中观察到。KCl的保护作用 对CA 1锥体神经元的作用也是明显的， 应用，虽然效果是双边的。 SD诱导3 在CACI前30天， 心脏骤停后24小时测试时，大鼠发生听源性癫痫发作（AuSz） 侮辱。 为了阐明SD的保护性质，将脑组织 在SD诱导后的不同时间间隔研究速率 并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的蛋白质合成 至SD，这仅在SD诱导3天的动物中得到证实 之前 处死大鼠蛋白质合成未见升高 SD诱导后1或7天以及所有对照组大鼠。