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目的：探讨钙及磷酯酶Ｃ（ＰＬＣ）在脑缺血再灌注损伤中的作用机制及ＰＬＣ抑制剂新霉素是否通过抑制ＰＬＣ活性而起脑保护作用。方法：用放血降压法建立大鼠全脑缺血模型，采用原子吸收光谱法及干湿法测定缺血再灌注后脑组织含钙量。含水量变化及新霉素对其影响。结果：再灌组含钙量、含水量较对照组升高（Ｐ＜０．０５）；再灌组内随灌注时间延长，脑组织含钙量、含水量增高（Ｐ＜０．０５）；给药组含钙量、含水量均较再灌组降低（Ｐ＜０．０５）。病理结果显示给药组细胞损伤、组织水肿程度较再灌组轻。结论：钙在脑缺血再灌注损伤中起重要作用，新霉素通过抑制ＰＬＣ活性而降低脑组组含钙量，减轻脑细胞损伤、组织水肿程度而起脑保护作用
Objective: To investigate the mechanism of action of calcium and phospholipase C (PLC) in cerebral ischemia-reperfusion injury and whether PLC inhibitor neomycin plays a protective role in brain through inhibiting PLC activity. Methods: The rat model of global cerebral ischemia was established by exsanguination and blood pressure reduction. The content of calcium in brain tissue after ischemia-reperfusion was determined by atomic absorption spectrometry and wet-dry method. Changes of water content and neomycin on it. Results: The contents of calcium and water in reperfusion group were higher than those in control group (P <0.05). The content of calcium and water in brain tissue increased with the prolongation of perfusion time in reperfusion group (P <0.05). The calcium content and water content in the administration group were lower than those in the reperfusion group (P <0.05). Pathological results showed that the drug-induced cell injury, tissue edema lighter than the reperfusion group. CONCLUSION: Calcium plays an important role in cerebral ischemia-reperfusion injury. Neomycin plays a neuroprotective role by inhibiting the activity of PLC and decreasing the content of calcium in brain tissue, reducing the degree of brain cell injury and tissue edema