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用4血管阻断法复制大鼠急性脑缺血再灌注动物模型，分别检测脑缺血再灌注过程中水、Ca2＋和MDA（丙二醛）含量及病理学改变以及尼莫地平对上述指标的影响。结果表明细胞内钙超载和自由基代谢紊乱在再灌注损伤中有协同作用．加重组织损伤，促进脑水肿；钙离子拮抗剂不仅具有钙拮抗作用，而且具有清除自由基作用，尼莫地平组与缺血再灌注组相比具有显著差异（P＜0.01），尼莫地平对急性脑缺血再灌注损伤具有保护作用。
The rat model of acute cerebral ischemia-reperfusion was reproduced by 4-vessel occlusion method. The contents of Ca2 +, MDA and the pathological changes of water, Ca2 + and MDA during cerebral ischemia-reperfusion were detected, and the effects of nimodipine on these indexes influences. The results show that intracellular calcium overload and free radical metabolism disorders have a synergistic effect in reperfusion injury. Increase the tissue damage and promote cerebral edema; calcium antagonists not only have calcium antagonism, but also have the role of scavenging free radicals, nimodipine group and ischemia-reperfusion group compared with the significant difference (P <0.01), nimodipine Acute cerebral ischemia-reperfusion injury has a protective effect.