中国病理生理杂志2001，Vol.17Issue(5)：451-454,4.
大鼠肢体缺血再灌注所致脑损伤及其机制探讨
Brain injury induced by ischemia-reperfusion of rat hindlimbs and its mechanisms
史中立 1凌立凌 1姚玉霞 1张爱子 1周君琳 1谷振勇 1黄新莉1
作者信息
摘要
Abstract
AIM:To investigate the pathologic changes in the brain and its underlying mechansims during ischemia-reperfusion of rat hindlimbs.METHODS:SD rats were divided into the normal(N), sham(S), 4 h ischemia without reperfusion(I), and 4 h ischemia-2, 6,12,18 or 24 h reperfusion (I-R) groups at random. Ischemia and ischemia-reperfusion were established with the occlusion or/and re-opening of the terminal of abdominal aorta, respectively. The pathologic changes in the brain tissue were morphologically observed. The expression of inducible nitric oxide synthase (iNOS) mRNA, and iNOS protein and the nitrotyrosine, a marker of peroxynitrite (ONOO-)，in the brain tissue were detected with RT-PCR and immunohistochemical technique, respectively. The brain superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectraphotometrically measured.RESULTS:Hydropic degeneration and severe injury to neurons were only showed in I-R group. Expressions of iNOS mRNA and protein were demonstrated in I-R, I and S groups, which were maximal in I-R 6 h group. iNOS positive neurons and microglias were more spread in I-R 6 h group than those in S and I groups. NT positive neurons were localized in the cerebral cortex and hippcampus of I-R 6 h group. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I-R 6 h group compared to the N, S and I groups. There were no significant changes in MDA and SOD in N, S and I groups.CONCLUSION:Severe ischemia-reperfusion of rat hindlimbs could induce brain injury, and its mechanisms might be related to enhanced expression of iNOS-NO-ONOO- in the brain.关键词
脑/四肢/局部缺血/再灌注损伤/一氧化氮分类
医药卫生引用本文复制引用
史中立,凌立凌,姚玉霞,张爱子,周君琳,谷振勇,黄新莉..大鼠肢体缺血再灌注所致脑损伤及其机制探讨[J].中国病理生理杂志,2001,17(5):451-454,4.
