脑梗塞的传统治疗方法是应用扩血管药物。Yamamoto[1]发现脑缺血后皿流重建可导致临床症状明显加重。自由基学说认为增加的脑血流为活性氧的产生提供了先决条件，由氧分子生成超氧阴离子自由基，后者对脑细胞膜具有强大的破坏作用。我们用Ca2+拮抗剂尼莫地平配合“仙台合剂”治 The traditional treatment of cerebral infarction is the application of vasodilator drugs. Yamamoto [1] found that reperfusion of the brain after cerebral ischemia can lead to significant clinical symptoms. Radical theory suggests that increased cerebral blood flow provides a prerequisite for the production of reactive oxygen species, which produce superoxide anion radicals from oxygen molecules, which have a powerful damaging effect on brain cell membranes. We use the Ca2 + antagonist nimodipine with “Sendai mixture” rule