Prevention of brain infarction by postischemic administration of histidine in rats
Prevention of brain infarction by postischemic administration of histidine in rats
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DOI：
10.1016/j.brainres.2005.01.061
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发表时间：
2005-03-28
期刊：
影响因子：
2.9
通讯作者：
Arai, T
中科院分区：
文献类型：
--
作者：
Adachi, N;Liu, K;Arai, T
通过阻塞右侧大脑中动脉造成局灶性脑缺血2 h，24 h后在大鼠脑中引起严重的脑梗死。再灌注后立即和6 h腹腔注射组胺前体组氨酸可减轻脑梗死。组氨酸（每次200 mg/kg、500 mg/kg和1000 mg/kg）组的梗死面积分别为对照组的71%、39%和7%。虽然侧脑室注射美托咪胺（3 nmol），一种H-1拮抗剂，并不影响组氨酸治疗大鼠的形态学结果，雷尼替丁（30 nmol），一种H-2拮抗剂，完全取消了组氨酸引起的缓解。这些发现表明，缺血后给予组氨酸可通过刺激中枢组胺H-2受体来预防脑梗死的发生。(c)2005 Elsevier B.V.保留所有权利。
Focal cerebral ischemia for 2 h by occlusion of the right middle cerebral artery provoked severe brain infarction in the rat brain after 24 h. Intraperitoneal administration of histidine, a precursor of histamine, immediately and 6 h after reperfusion, alleviated brain infarction. The infarct size in the histidine (200 mg/kg, 500 mg/kg, and 1000 mg/kg, each time) groups was 71%, 39%, and 7% of that in the control group, respectively. Although intracerebroventricular administration of mepyramine (3 nmol), an H-1 antagonist, did not affect the morphologic outcome in histidine-treated rats, ranitidine (30 nmol), an H-2 antagonist, completely abolished the alleviation caused by histidine. These findings indicate that postischemic administration of histidine prevents development of brain infarction by stimulating central histamine H-2 receptors. (c) 2005 Elsevier B.V. All rights reserved.