Katayama Y, Kawamata T, Maeda T, Ishikawa K, Tsubokawa T
Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.
Brain Res. 1994 Jan 28;635(1-2):331-4. doi: 10.1016/0006-8993(94)91457-5.
In order to determine the role of excitatory amino acids (EAAs) in free fatty acid (FFA) liberation during cerebral ischemia, we examined the effect of in situ administration of kynurenic acid, a broad-spectrum antagonist of EAA receptors, by microdialysis on the increase in FFA levels during ischemia in the rat hippocampus. A transient rapid increase in FFA levels, superimposed on a continued slow increase, was observed beginning at 1-2 min after ischemia induction. The early rapid increase in FFAs was profoundly inhibited by kynurenic acid, suggesting that EAAs are critically involved in the early phase of FFA liberation. Development of massive ionic shifts during cerebral ischemia can be delayed for several minutes by kynurenic acid administered by the same procedure, suggesting a vital role for EAAs in the early appearance of anoxic depolarization. The observed inhibition of early FFA liberation may thus be attributable to the delay in development of massive ionic shifts and resultant neurotransmitter release which may activate phospholipase A2 and C.
为了确定兴奋性氨基酸（EAA）在脑缺血期间游离脂肪酸（FFA）释放中的作用，我们通过微透析研究了原位给予犬尿氨酸（一种EAA受体的广谱拮抗剂）对大鼠海马缺血期间FFA水平升高的影响。在缺血诱导后1 - 2分钟开始观察到，FFA水平出现短暂的快速升高，并叠加在持续的缓慢升高之上。犬尿氨酸可显著抑制FFA早期的快速升高，这表明EAA在FFA释放的早期阶段起着关键作用。通过相同程序给予犬尿氨酸，可使脑缺血期间大量离子转移的发生延迟几分钟，这表明EAA在缺氧去极化的早期出现中起着重要作用。因此，观察到的早期FFA释放受抑制现象可能归因于大量离子转移和由此导致的神经递质释放的延迟，而神经递质释放可能会激活磷脂酶A2和C。
