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目的观察赛庚啶的脑保护作用，并初步探讨其作用机制。方法采用Ｐｕｌｓｉｎｅｌｉ四动脉结扎法制作大鼠急性前脑缺血再灌注损伤的模型。结果缺血再灌注造成脑组织严重损伤，脑水分、脑钙及ＭＤＡ含量显著增高，脑组织ＬＤＨ含量明显减少，脑电图严重抑制，锥体细胞坏死。赛庚啶能剂量依赖性地逆转上述变化。结论赛庚啶具有明显的脑保护作用，其机制可能与其钙拮抗作用和抗氧化作用有关。
Objective To observe the protective effect of cyproheptadine and to explore its mechanism. Methods The model of acute forebrain ischemia-reperfusion injury in rats was made by Pulsineli four-artery ligation. Results Severe cerebral injury was induced by ischemia-reperfusion. The contents of water and brain calcium and MDA were significantly increased. The content of LDH in brain tissue was significantly decreased. EEG was severely inhibited and pyramidal cell necrosis was observed. Cyproheptadine reverses these changes in a dose-dependent manner. Conclusion cyproheptadine has obvious brain protective effect, its mechanism may be related to its calcium antagonism and anti-oxidation.