Candesartan reduces superoxide production after global cerebral ischemia

被引：32

作者：

Sugawara, T ^{[1
]}

Kinouchi, H ^{[1
]}

Oda, M ^{[1
]}

Shoji, H ^{[1
]}

Omae, T ^{[1
]}

Mizoi, K ^{[1
]}

机构：

[1] Akita Univ, Sch Med, Dept Neurosurg, Akita 0108543, Japan

来源：

NEUROREPORT | 2005年 / 16卷 / 04期

关键词：

angiotensin II; angiotensin receptor; global cerebral ischemia; superoxide;

D O I：

10.1097/00001756-200503150-00004

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Excessive superoxide production after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type I receptor activation results in production of superoxide, but whether angiotensin II type I receptor blockade prevents production of superoxide and subsequent neuronal injury after ischemia remains unclear. Normotensive rats received the angiotensin II type I receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CAI neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production was significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type I receptor may have an essential role in superoxide production and subsequent injury in vulnerable neurons after global cerebral ischemia. NeuroReport 16:325-328 (c) 2005 Lippincott Williams & Wilkins.

引用

页码：325 / 328

页数：4

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