电刺激一侧颈上神经节后家兔海马CA1区腺苷及其代谢物含量的变化(英文)

CHANGES IN CONTENTS OF ADENOSINE AND ITS METABOLITES IN THE RABBIT HIPPOCAMPAL CA1 AFTER ELECTRICAL STIMULATION OF THE UNILATERAL SUPERIOR CERVICAL GANGLION

脑缺血由电刺激家兔一侧颈上神经节诱发。腺苷（Adenosine,Ado）及其代谢物在两侧海马CA1区细胞外的含量采用在体微透析技术结合高效液相色谱法（HPLC）监测。伴随着电刺激，在与刺激同侧的海马CA1区细胞外，腺苷、肌苷（Inosine，Ino）和次黄嘌吟（Hypoxanthine,Hyp）的含量分别显著性地提高了6．5倍(Ado）、4．5倍（Ino）和2．3倍（Hyp）（P＜0．05），而黄嘌呤（Xanthine,Xan）的含量在刺激期间没有改变，但停止刺激后暂时性地上升了3.3倍（P＜0．05）。这些结果与我们先前报道的电生理学及病理学结果相一致。本结果表明，腺苷可能是在脑缺血的早期起神经保护作用，而伴随黄嘌呤形成过程所产生的有害自由基离子，可能对这一不完全脑缺血模型缺血后脑损伤的形成是重要的。

Cerebral ischemia was induced by electrical stimulation of the rabbit unilateral superior cervicalganglion. Extracellular (EC) contents of adenocine (Ado) and its metabolites in the bilateral hippocampal CA1were monitoed by in vivo micndialysis combined with high Performance liquid chromatography (HPLC) method.Following electrical stimulation, EC contents of Ado, inosine (Ino) and hypoxanthine (Hyp) were significantlyincreased 6. 5-fold (Ado), 4. 5-fold (Ino) and 2. 3-fold (Hyp) in the hippocampal CA1 on ipsilateral side tostimulation, respectively (P < 0. 05 ), while the content of xanthine (Xan) was found unaltered during stimulationbut transiently increased 3. 3-fold after stoppage of stimulation (P < 0. 05). These results are consistent with ourelectrophysiologcal and pathological findings previously reported and indicate that Ado might play a neuroprotective role in the early period of ischemia and that harmful free radicals are released when Xan is formed by xanthineoxidase, which could be important for development of postischemic cerebral injuries in this animal model of incomplete cerebral ischemia.