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氟桂利嗪缺血后治疗改善缺血性脑损伤。

Amelioration of ischaemic brain damage by postischaemic treatment with flunarizine.

作者信息

Deshpande J K, Wieloch T

出版信息

Neurol Res. 1985 Mar;7(1):27-9. doi: 10.1080/01616412.1985.11739696.

Abstract

The effect of flunarizine, a calcium entry blocker, on ischaemic damage was investigated using a new model of forebrain ischaemia. Fasted rats were subjected to nine minutes ischaemia and one week recovery. One group served as control; a second was pretreated orally with flunarizine; a third group received postischaemic flunarizine treatment. Focussing on the hippocampus, an area of high susceptibility to ischaemic damage, we report that flunarizine treatment significantly reduced neuronal necrosis. Importantly, the amelioration of necrosis was also observed when flunarizine was administered 5 min following resumption of cerebral perfusion.

摘要

使用一种新的前脑缺血模型,研究了钙通道阻滞剂氟桂利嗪对缺血性损伤的影响。将禁食大鼠进行9分钟的缺血和1周的恢复。一组作为对照;第二组口服氟桂利嗪进行预处理;第三组在缺血后接受氟桂利嗪治疗。聚焦于对缺血性损伤高度敏感的海马区,我们报告氟桂利嗪治疗显著减少了神经元坏死。重要的是,在恢复脑灌注后5分钟给予氟桂利嗪时,也观察到坏死的改善。

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