不完全脑缺血期间家兔尾核与大脑皮质区细胞外腺苷的变化

Changes in extracellular adenosine in the rabbit striatum and cerebral cortex during incomplete cerebral ischemia

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。

Microdialysis probes were implanted into the rabbit cerebral cortex and caudate nucleus followed by perfusion with Ringer solution at a flow rate of 3.0μl/min. Cerebral ischemia was induced by electrical stimulation of the unilateral superior cervical ganglion for 1h. Dialysate samples were analyzed by high performance liquid chromatography (HPLC). Following ischemia, extracelluar (EC) contents of adenosine (Ado) and its metabolites were significantly increased upto 6 ～ lOfold(Ado), 5 ～ 6fold(Inosine, Ino) and 2 ～ 3fold(Hypoxanthine, Hyp) in both the cerebral cortex and caudate nucleus(P<0.05), respectively, while xanthine(Xan) contents rose 3.8 - 4.4 times during the early period of postischemia (P<0.05). These results suggest a significant accumulation of oxypurines in the interstitium during ischemia and the presence of an activity of xanthine oxidase in brain tissue.