脑缺血对大鼠循环铁的影响

目的 探讨脑缺血对大鼠循环铁的影响。方法 雄性Wistar大鼠随机分为脑缺血1、3、7、28d和假手术组；脑缺血组结扎双侧颈总动脉造成大鼠脑缺血，假手术组仅分离出双侧颈总动脉但不结扎；采用比色法测定大鼠血清铁含量；用放射免疫法测定血清铁蛋白含量。结果脑缺血1d大鼠血清铁含量低于假手术组（P〈0．05）；缺血3d血清铁含量虽低于假手术组，但无统计学意义（P〉0．05）；之后随着缺血时间的延长血清铁含量呈增高趋势，缺血28d时显著高于假手术组（P〈0．01）。脑缺血1d大鼠血清铁蛋白含量与假手术组比较无明显差别（P〉0．05）；缺血3d组低于假手术组（P〈0．05）；之后随着缺血时间的延长血清铁蛋白含量呈增高趋势，在缺血7、28d时均高于假手术组（P〈0．05）。结论脑缺血早期引起大鼠循环铁降低，晚期升高；循环铁的改变可能参与了脑铁含量升高和神经元铁沉积过程。

Changes of circulation iron level induced by cerebral isehemia in rats

Objective To study changes of circulation iron level mduced by cerebral iscneima in rats. Methods Male Wistar rats were randomly divided into sham and cerebral ischemia groups. Further, cerebral ischemia groups subdivided by different ischemic time. The cerebral ischemia was induced by ligating bilateral common carotid arteries with silk in rats. The sham group was received sham operation. Serum iron concentration was measured by colorimetric method, and serum ferritin concentration was measured by radioirmmunoassay. Results Serum iron concentration in rats suffering from cerebral ischemia for 1 day decreased compared with sham group （P〈0. 05）. Serum iron concentration in rats suffering from the cerebral ischemia for 3 days was lower than sham group, it was not obviously significant （P〉0. 05）. Serum iron concentration in cerebral ischemic rats increased following ischemia. It reached a top concentration at the 28th day of ischemia（P〈0. 01）. Similarly, serum ferritin concentration in rats suffering from cerebral ischemia for 1 day was not significant difference. Serum ferritin concentration of rats suffered from cerebral ischemia for 3 days decreased as compared with sham rats （P〈0. 05）. Subsequently, Serum ferritin concentration of cerebral ischemic rats increased, and was higher at the 7th and 28th day than sham group （P〈0. 01 ）. Conclusions Serum iron and ferritin concentration decreased during earlier period of cerebral ischemia, whereas increased following a prolonging of ischemia. The change of circulation iron level may involve in iron deposition in neuron by induced cerebral ischemia.