摘要
目的 :从ATP酶活性变化和自由基损伤方面研究老龄大鼠脑缺血再灌注损伤的机制。方法 :青年(5月龄 )和老龄 (2 0月龄以上 )大鼠均分为模型组和正常对照组 ,观察大鼠全脑缺血 30min再灌注 6 0min后ATP酶和SOD活性及MDA、Ca2 + 、Na+ 、K+ 含量。结果 :老龄模型组Ca2 + 水平高于青年模型组和老龄对照组。老龄对照组脑组织Na+ -K+ -ATP酶低于青年对照组 ,老龄模型组低于青年模型组。老龄对照组Ca2 + -ATP酶低于青年对照组 ,老龄模型组低于青年模型组但高于老龄对照组。老龄对照组血清和脑组织中SOD活性低于青年对照组 ,老龄模型组低于青年模型组。老龄模型组血清和脑组织MDA/SOD比值高于老龄对照组。结论 :脑缺血再灌注损伤与钙超载和自由基损伤有关 ,但由于老龄大鼠脑组织ATP酶和钙含量及自由基代谢的增龄变化 ,使脑缺血再灌注后这些病理改变较青年大鼠更为明显并具有一定特点。
AIM: To study the mechanism of brain ischemia-reperfusion injury from ATPase activity and free radical metabolism in aged rats. METHODS: The young rats (5 months) and the aged rats (more than 20 months) were divided into young control group(YCG), young model group(YMG), aged control group(ACG) and aged model group(AMG). The ATPase and SOD activities and the contents of MDA, Ca 2+ , Na + and K + were measured in the rats with 30 min brain ischemia followed by 60 min reperfusion. RESULTS: The Ca 2+ content in the AMG was higher than that in the YMG and the ACG. The Na +-K +-ATPase activity in the ACG was lower than that in the YCG,was lower in the AMG than that in the YMG . The Ca 2+ -ATPase activities in the YCG was higher than that in the ACG, was lower in the AMG than that in the YMG and was higher than the ACG's. The serum and brain tissue SOD activities in the ACG was lower than that in the YCG, was lower in the AMG than YMG 's. The serum and brain tissue MDA/SOD ratio in the AMG was higher than that in the ACG. CONCLUSION: The brain tissue ischemia- reperfusion injury was related with calcium overload and free radical injury. The pathological changes were obvious and had some characteristics in the aged rats compared with the young rats because of the brain tissue aging changes in ATPase,calcium content and free radical metabolism in the aged rats.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第11期1052-1055,共4页
Chinese Journal of Pathophysiology
基金
河南省杰出青年基金资助 (1999- 0 5 )
