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实验在新西兰白兔上进行,不完全脑缺血由电刺激一侧颈上神经节1小时诱发。采用微透析技术测定家兔纹状体及大脑皮质区细胞外(Extracellular,EC)腺苷(Adenosine,Ado)及代谢物的水平。微透析探头埋入侧尾核及大脑皮质区,随后以3.0μl/min速度灌流Ringer液。透析样品用高效液相色谱法(HPLC)分析。随着不完全脑缺血,Ado及代谢物的EC含量明显增高,在侧尾核区分别提高了10倍(Ado)、6倍(肌苷Inosine,Ino)和3倍(次黄嘌呤Hypoxanthine,Hyp),在大脑皮质区分别提高了6倍(Ado)、5倍(Ino)和2倍(HyP)(P<0.05)。黄嘌呤(Xanthine,Xan)的含量在缺血期间没 有改变,但在缺血后暂时地上升。这些结果提示,黄嘌呤形成过程中产生的有害自由基离子对于这一不完全脑缺血模型中,脑内缺血样损伤的形成也许是重要的。
Experiments in New Zealand White rabbits, incomplete cerebral ischemia by electrical stimulation of the superior cervical ganglion for 1 hour induced. Microdialysis was used to determine the level of extracellular (Adenosine, Ado) and metabolites in the striatum and cerebral cortex of rabbits. Microdialysis probes were embedded in the caudate nucleus and cerebral cortex, followed by perfusion of Ringer’s solution at 3.0 μl / min. Dialysis samples were analyzed by high performance liquid chromatography (HPLC). With incomplete cerebral ischemia, the ECs of Ado and its metabolites were significantly increased, with Ado, 6-fold (Inos) and 3-fold (Hypoxanthine, Hyp) increased 6-fold (Ado), 5-fold (Ino) and 2-fold (HyP) in the cerebral cortex (P <0.05). Xanthine (Xan) levels did not change during ischemia, but temporarily increased after ischemia. These results suggest that deleterious free radical ions produced during the xanthine formation may be important for the formation of ischemic lesions in the brain in this incomplete cerebral ischemia model.