大鼠MCA闭塞再循环模型中LCGU和rCBF的变化及新型自由基清除剂MCI-186的改善作用。

S Yuki, K Kogure
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引用次数: 2

摘要

我们观察了大脑中动脉闭塞或再循环模型大鼠脑血流(rCBF)和局部脑葡萄糖利用(LCGU)的变化,并检测了自由基清除剂3-甲基-1-苯基吡唑龙-5- 1 (MCI-186)的抗缺血作用。经再循环后,大脑前动脉供血皮层LCGU明显升高。这种葡萄糖的高代谢至少部分是由缺血后氧化损伤引起的,因为MCI-186改善了该区域的高LCGU。这些结果提示这种类型的自由基清除剂对抑制缺血后损伤的有效性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The changes of LCGU and rCBF in the MCA occlusion-recirculation model in rats and the ameliorating effect of MCI-186, a novel free radical scavenger.

We examined the change of regional cerebral blood flow (rCBF) and local cerebral glucose utilization (LCGU) in the middle cerebral artery (MCA) occlusion or recirculation model of rats, and tested anti-ischemic effects of a free radical scavenger, 3-methyl-1-phenyl-pyrazolon-5-one (MCI-186). A remarkable increase in LCGU was observed in the cortex supplied by the anterior cerebral artery after recirculation. This hypermetabolism of glucose was at least partly caused by the postischemic oxidative injury, since MCI-186 ameliorated the high LCGU in this area. These results suggested the usefulness of this type of free radical scavenger for inhibiting the postischemic injury.

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