【摘要】 目的　从 ATP酶活性变化和自由基损伤方面研究老年大鼠脑缺血再灌注肾脏损伤机制。方法　青年 (5～ 6月龄 )和老年 (2 0～2 2月龄 )大鼠均分为模型组和正常对照组 ,观察大鼠全脑缺血 30 min再灌注 60 min后肾脏组织形态和肌酐 (Cr)、尿素氮 (BUN)、丙二醛(MDA)含量及超氧化物岐化酶 (SOD)、ATP酶的活性。结果　青年和老年模型组大鼠肾脏组织形态和功能均出现明显的病理改变 ,老年模型组较青年模型组严重。青年模型组和老年模型组肾脏组织 MDA含量和 MDA/SOD比值分别高于青年对照组和老年对照组。老年模型组肾脏组织Na+ - K+ - ATP酶和 Ca2 + - ATP酶活性低于青年模型组 ;老年对照组肾脏 Ca2 + - ATP酶活性低于青年对照组 ,老年模型组肾脏 Ca2 + - ATP酶活性低于老年对照组。结论　脑缺血再灌注肾脏损伤老年大鼠较青年大鼠严重 ,ATP酶活性降低和自由基损伤可能是其主要机制之一。由于老年大鼠 ATP酶活性和自由基代谢的增龄变化使这些病理改变较青年明显并具有一定特点。更多还原

【Abstract】 Objectives To study the mechanism of kidney injury after brain ischemia reperfusion in aged rats from the changes of ATP ase activity and the free radical injury. Methods Young (5 months) and aged (20 months or more) rats were divided into model groups and control groups respectively. It was studied that the following items in rats with 60 min reperfusion after 30 rain brain ischemia: the activity of ATP ase and superoxide dismutase(SOD), the contents of creatinine(Cr), urea nitrogen(BUN), MDA. Results The kidney tissue pathological injury was found in two model’s, especially aged model’s. The kidney MDA content and MDA/SOD ratio was higher in the young model’s and aged model’s than those in the young control’sand aged control’s. The activity of kidney Na + K + ATP ase and Ca 2+ ATP ase in the aged model’s was lower than those in the young model’s. The activity of kidney Ca 2+ ATP ase was lower in the aged control’s than that in the young control’s, was lower in aged model’s than that in the aged control’s. Conclusions The kidney injuryafter brain ischemia reperfusion in aged rats was more serious than that in the young tats. The change of ATP ase activity and injury of free radical might be one of the primary mechanisms. With the aging change of ATP ase activity and free radical metabolism these pathological change were obvious and distinctive in aged ratscompared with that in the young rats.更多还原