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了解铁负荷与急性肾缺血损伤的关系。方法给铁负荷组大鼠连续５日每日腹腔内注射次氮基三乙酸亚铁，对照组予等量次氮基三乙酸或生理盐水。结果实验第７天，铁负荷组肾脏铁含量较正常对照组增加了７２％，还原型谷胱甘肽含量则明显下降，但无显著肾脏形态或功能改变。肾脏缺血４０分钟并再灌注１小时后，铁负荷组肾脏菊糖清除率为０．２２±０．１０ｍｌ／ｍｉｎ，显著低于两对照组。再灌流２４小时后，铁负荷组肾脏组织形态学半定量积分高于后两组。仅铁负荷组大鼠肾再灌注１５分钟时皮质丙二醛含量显著高于缺血前水平。结论早期小剂量铁负荷增加肾脏对缺血后再灌注损伤的易感性，其机理与加强肾脏自身氧化及损伤其抗氧化能力有关。
To understand the relationship between iron overload and acute renal ischemia injury. Methods The rats in iron load group were injected intraperitoneally with iron nitrilotriacetate for 5 consecutive days and the control group with equal amount of nitrilotriacetic acid or normal saline. Results On the 7th day of experiment, the content of iron in kidneys increased by 72% and the content of reduced glutathione decreased significantly in the iron-loaded group compared with the normal control group, but there was no significant change in kidney morphology or function. Renal ischemia for 40 minutes and 1 hour after reperfusion, renal iron clearance rate of inulin 0.22 ± 0.10ml / min, significantly lower than the two control groups. After 24 hours of reperfusion, the semi-quantitative integral of renal histomorphology in the iron overload group was higher than the latter two groups. The iron content of cortical malondialdehyde was significantly higher than that of the pre-ischemic rats at 15 minutes after renal reperfusion in iron-only rats. Conclusion Early low-dose iron loading increases the susceptibility of the kidney to ischemia-reperfusion injury, and its mechanism is related to the enhancement of kidney’s own oxidation and the impairment of its antioxidant capacity.