脑缺血再灌注期间海马CA1区细胞色素氧化酶活性的变化

目的观察脑缺血再灌注后海马CA1区细胞色素氧化酶活性的变化.方法沙土鼠前脑缺血再灌注模型,运用酶组织化学方法结合计算机图像分析,测定脑缺血再灌注6h、2d、4d海马CA1区细胞色素氧化酶的活性,应用高效液相紫外监测器测定海马ATP、ADP、AMP含量.结果随着再灌注时间的延长,海马CA1区细胞色素氧化酶活性呈进行性下降的趋势,再灌注4d时降至假手术组的51%(P<0.01).海马ATP含量的变化与细胞色素氧化酶活性的变化一致.结论脑缺血再灌注损伤的机制可能与细胞色素氧化酶活性下降导致的细胞能量代谢障碍有关.

Changes of activity of cytochrome oxidase in the hippocampus CA1 sector following cerebral ischemia/reperfusion

Objective To investigate the change of the activity of cytochrome oxidase in the hippocampus CA1 sector following cerebral ischemia/reperfusion.?Methods The gerbil cerebral ischemia model was prepared by occluding bilateral carotid arteries. The activity of cytochrome oxidase in the hippocampus CA1 sector was determined 6 h, 2 d, 4 d after reperfusion by using enzyme histochemical staining coupled with computer image analysis system. The ATP level in hippocampus was measured by high performance liquid chromatography (HPLC).?Results The activity of cytochrome oxidase in the hippocampus CA1 sector was progressively decreased during reperfusion, and on the 4 d after reperfusion, reached 51% that of the sham operation group. The ATP level in the hippocampus changed consistently with the activity of cytochrome oxidase.?Conclusion The mechanism of cerebral ischemia/reperfusion injury may be related to the failure of energy metabolism secondary to the inhibition of the activity of cytochrome oxidase.