缺血再灌注时大鼠脑细胞外液中腺苷含量的变化及巴曲酶的影响

动态观察脑缺血及再灌注时鼠脑细胞外液中腺苷及其代谢产物的变化规律以及巴曲酶对此的影响。方法在大鼠四血管结扎缺血再灌注模型上，用微透析及高效液相色谱技术测定在缺血及再灌注时各时间点脑细胞外液中腺苷及其代谢产物的含量。结果对照组的腺苷、肌苷（Ｉｎｏ）、次黄嘌呤（Ｈｙｐ）、黄嘌呤（Ｘａｎ）在缺血和再灌注后的各时间点均显著升高。腺苷出现２个高峰，分别在缺血后２０分钟及再灌注１５分钟时，到再灌注６０分钟又回落到接近基础灌流水平。Ｉｎｏ、Ｈｙｐ及Ｘａｎ只在再灌注３０分钟时出现１个高峰，到再灌注６０分钟仍滞留在较高水平。巴曲酶组腺苷、Ｉｎｏ、Ｈｙｐ及Ｘａｎ的变化规律与对照组相同，但升高的幅度低于对照组。结论脑缺血及再灌注损伤时腺苷的水平明显升高，呈现缺血及再灌注时的２个高峰。腺苷代谢产物的升高时间略滞后，仅在再灌注３０分钟时达峰值。巴曲酶可抑制腺苷及其代谢产物的升高，可能与其减轻损伤程度有关

The in vivo changes of extracellular fluid adenosine on brain ischemia/reperfusion and the effects of batroxobin on these changes in rats

Objective To monitor the changes of adenosine and its metabolites in extracellular fluid (ECF) of brain ischemia/reperfusion rats in vivo and the effects of batroxobin on them. Methods Using microdialysis and high performance liquid chromatography ultraviolet (HPLC UV) technique to detect continuously the concentrations of adenosine (Ade), inosine (Ino), hypoxanthine (Hyp) and xanthine (Xan) in ECF of the striatum after ischemia and reperfusion in four vessel occlusion model of Wistar rats. Batroxobin (8 BU/kg) was given intravenously 15 min before ischemia.Results In the control group, the concentration of Ade, Hyp, Ino and Xan in ECF increased significantly after ischemia and reperfusion. Two peak levels of Ade were detected, one reached 20 min after four vessel occlusion, and another occurred at 30 min after reflow. Ade concentration dropped to basic level at 60 min after reperfusion. The elevations of Ino, Hyp and Xan concentrations had only one peak at 30 min after reflow, and remained higher than the basic levels at 60 min after reperfusion. Batroxobin could decrease the ECF levels of Ade, Ino, Hyp and Xan during ischemia and reperfusion.Conclusion The concentration of adenosine in ECF might significantly increased in brain ischemia/reperfusion injury, and the two peak levels might be reached in ischemia and reperfusion periods respectively. Batroxobin could inhibit the increase of adenosine and its metabolites, and that might be related to its neuroprotective effects in ischemia/reperfusion injury.