Effects of naloxone on lactate, pyruvate metabolism and antioxidant enzyme activity in rat cerebral ischemia/reperfusion

被引：61

作者：

Chen, CJ ^{[1
]}

Cheng, FC ^{[1
]}

Liao, SL ^{[1
]}

Chen, WY ^{[1
]}

Lin, NN ^{[1
]}

Kuo, JS ^{[1
]}

机构：

[1] Taichung Vet Gen Hosp, Dept Educ & Res, Taichung 40705, Taiwan

来源：

NEUROSCIENCE LETTERS | 2000年 / 287卷 / 02期

关键词：

energy metabolism; free radical; microdialysis; opioid antagonist; opioid peptide; stroke;

D O I：

10.1016/S0304-3940(00)01151-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Whether naloxone may modulate energy metabolism and endogenous antioxidant enzyme activities in ischemic cortex was studied. Cerebral ischemia/reperfusion (I/R) was produced by occluding two common carotid arteries and the right middle cerebral artery for 90 min followed by reperfusion in anesthetized Sprague-Dawley rats. Both pretreatment (0.03 or 0.3 mg) and post-treatment (0.3 mg) of naloxone by intracerebroventricular infusion significantly reduced cortical infarct volumes. Pre-treatment with 0.03 mg reduced ischemia-induced suppression of extracellular pyruvate level and enhancement of lactate/pyruvate ratio as well as cerebral I/R-induced increases of endogenous catalase, glutathione peroxidase, and manganese superoxide dismutase activities. In conclusion, neuroprotective effects of naloxone in terms of reducing brain infarction involve attenuation of the disturbance of cellular functions following cerebral I/R via restoration of mitochondrial activities or energy metabolism. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：113 / 116

页数：4

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