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超氧化物歧化酶活性降低与局灶性缺血大鼠脑T2加权磁共振成像显示的水肿相关。

Reduction of superoxide dismutase activity correlates with visualization of edema by T2-weighted MR imaging in focal ischemic rat brain.

作者信息

Imaizumi S, Chang L, Cohen Y, Chan P H, Weinstein P R, Yoshimoto T, James T L

机构信息

CNS Injury and Edema Research Center, University of California, San Francisco.

出版信息

Neurol Med Chir (Tokyo). 1994 Jan;34(1):1-9. doi: 10.2176/nmc.34.1.

DOI:10.2176/nmc.34.1
PMID:7514745
Abstract

This study investigated the correlation between in vivo serial T2-weighted magnetic resonance (MR) imaging and changes in superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and water, sodium ion (Na+), and potassium ion (K+) contents measured in vitro using rat brain following right middle cerebral artery occlusion in conjunction with bilateral common carotid artery (CCA) occlusion. One hour later the left CCA was released. Serial MR images showed edema developed from the outer cortex towards the center. The T2 signal intensity of the injured right cortex increased with time compared to that of the contralateral cortex. Increased Na+ and water and decreased K+ contents occurred in the injured cortex, indicating that serial T2-weighted MR imaging reflects the changes in water content and Na+ and K+ concentrations determined by biochemical techniques. GSH-Px activity was little changed. Total SOD in the injured cortex decreased 1 hour after ischemia and remained low throughout the experiment. In contrast, SOD activity in the noninfarcted left cortex also decreased after 1 hour but returned to normal after 2 hours of ischemia. Our results suggest that oxygen free radicals are important in developing ischemic brain edema and cerebral infarction.

摘要

本研究调查了在大鼠大脑右侧大脑中动脉闭塞并伴有双侧颈总动脉(CCA)闭塞后,体内连续T2加权磁共振(MR)成像与超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性变化以及体外测量的水、钠离子(Na+)和钾离子(K+)含量之间的相关性。一小时后松开左侧颈总动脉。连续MR图像显示水肿从外侧皮质向中心发展。与对侧皮质相比,受损右侧皮质的T2信号强度随时间增加。受损皮质中Na+和水含量增加,K+含量降低,表明连续T2加权MR成像反映了通过生化技术测定的水含量以及Na+和K+浓度的变化。GSH-Px活性变化不大。受损皮质中的总SOD在缺血1小时后降低,并在整个实验过程中保持较低水平。相比之下,未梗死的左侧皮质中的SOD活性在缺血1小时后也降低,但在缺血2小时后恢复正常。我们的结果表明,氧自由基在缺血性脑水肿和脑梗死的发生发展中起重要作用。

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