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脑缺血期间游离脂肪酸的释放和细胞肿胀:兴奋性氨基酸的作用。

Free fatty acid liberation and cellular swelling during cerebral ischemia: the role of excitatory amino acids.

作者信息

Katayama Y, Kawamata T, Maeda T, Tsubokawa T

机构信息

Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Acta Neurochir Suppl (Wien). 1994;60:242-5. doi: 10.1007/978-3-7091-9334-1_64.

DOI:10.1007/978-3-7091-9334-1_64
PMID:7976556
Abstract

We previously demonstrated the occurrence of cellular swelling during cerebral ischemia in vivo using microdialysis. 14C-Sucrose was pre-perfused into the extracellular space (ECS) as an ECS marker, and cellular swelling was detected as an increase in extracellular concentration of 14C-sucrose. In the present study, we examined in rats the time courses of the increase in FFA in relation to the occurrence of cellular swelling, and the role of excitatory amino acids (EAAs) in these events. A pair of microdialysis probes were placed in the hippocampus bilaterally. One probe was perfused with modified Ringer solution containing kynurenic acid (KYN, 10 mM), a broad-spectrum EAA antagonist, and the other with Ringer solution as a control. At 30 minutes after the initiation of perfusion, ischemia was induced by decapitation. The brain was subjected to microwave irradiation at 0-8 minutes after decapitation, and the FFA levels in the dorsal hippocampus were measured by high performance liquid chromatography. The time course of cellular swelling was determined in a separate group of animals using the previously described method. It was found that arachidonic and stearic acids began to demonstrate a rapid increase during the period from 1 to 2 minutes following ischemia induction. The levels of oleic and palmitic acids demonstrated similar but less marked increase. The rate of increase became less rapid after 4 minutes, suggesting a transient rapid increase superimposed on a background slow increase. The rapid increase roughly corresponded in timing to the occurrence of the early cellular swelling.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们之前利用微透析技术在体内证明了脑缺血期间细胞肿胀的发生。将14C-蔗糖预先灌注到细胞外间隙(ECS)作为ECS标志物,细胞肿胀表现为14C-蔗糖细胞外浓度升高。在本研究中,我们在大鼠中研究了游离脂肪酸(FFA)升高与细胞肿胀发生的时间进程,以及兴奋性氨基酸(EAA)在这些事件中的作用。将一对微透析探针双侧置于海马体中。一个探针用含有犬尿烯酸(KYN,10 mM)的改良林格氏液灌注,KYN是一种广谱EAA拮抗剂,另一个探针用林格氏液作为对照。灌注开始30分钟后,通过断头诱导缺血。断头后0 - 8分钟对大脑进行微波照射,并用高效液相色谱法测量背侧海马体中的FFA水平。使用先前描述的方法在另一组动物中确定细胞肿胀的时间进程。结果发现,花生四烯酸和硬脂酸在缺血诱导后1至2分钟内开始迅速升高。油酸和棕榈酸水平呈现类似但不太明显的升高。4分钟后升高速度变慢,表明在背景缓慢升高的基础上有短暂的快速升高。快速升高的时间大致与早期细胞肿胀的发生时间一致。(摘要截断于250字)

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