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作 者:崔景斌[1] 王俊萍[1] 鄢文海[2] 赵卫星[1] 白浩[1]
机构地区:[1]郑州大学基础医学院生物化学教研室,郑州450052 [2]郑州大学基础医学院病理生理学教研室,郑州450052
出 处:《郑州大学学报(医学版)》2002年第2期169-171,共3页Journal of Zhengzhou University(Medical Sciences)
基 金:河南省科技攻关基金资助项目 0 0 1170 80 5
摘 要:目的 :通过测定大鼠脑缺血再灌注后兴奋性氨基酸 (EAA)、一氧化氮合酶 (NOS)和一氧化氮 (NO)含量的变化 ,探讨脑缺血再灌注损伤的发生机制。方法 :将动物分为假手术组和缺血 30min后再灌注组 ,通过高效液相色谱或分光光度法测定再灌注后不同时间 (1h、6h、2 4h、4 8h和 72h)脑组织EAA、NOS和NO的含量。结果 :再灌注后 1hEAA水平较假手术组显著增高 ,以谷氨酸最为明显 ,随后逐渐下降 ,2 4h达正常水平。NOS和NO于再灌注后1h即升高 (P <0 .0 5 ) ,2 4h达最高水平 (P <0 .0 1) ,72h降至正常。结论 :脑缺血再灌注后EAA、NOS和NO含量发生变化 。Aim:To study the mechanism of cerebral ischemia reperfusion injury(IRI) by observing the changes of excitatory amino acid(EAA),nitric oxide synthase(NOS), and nitric oxide(NO) levels in rat brain after IRI. Methods: The animal models of the sham operation and reperfusion after cerebral ischemia were made. The levels of EAA, NOS, and NO were measured by high performance liquid chromalographic determination or spectrophotography at different times(1 h,6 h,24 h,48 h and 72 h) after IRI. Results: Compared to sham operation group, EAA level was increased significantly at 1h after IRI, especially for glutamic acid, and then was declined gradually to normal level at 24 h. NOS and NO concentrations were increased significantly( P < 0.05) at 1 h after IRI, then reached the highest levels ( P <0.01) at 24 h after IRI and at last was declined to normal level at 72 h. Conclusion:IRI could cause EAA,NOS and NO content changes in rats and the changes might be closely related to cerebral ischemia reperfusion.
关 键 词:再灌注损伤 兴奋性氨基酸 一氧化氮合酶 一氧化氮 大鼠 脑缺血
分 类 号:R743.31[医药卫生—神经病学与精神病学]
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