深低温停循环下尼莫地平的大鼠脑保护作用研究

目的 研究深低温停循环（DHCA）下尼莫地平对全脑缺血再灌注损伤的保护作用及其机制.方法 将96只DHCA模型SD雄性大鼠随机均分为模型组（DHCA）和尼莫地平组（DHCA＋尼莫地平）,每组48只,采用二血管阻断加低血压法制作全脑缺血再灌注模型.每组根据时相再分为缺血后再灌注0h（T1）、2h（T2）、6h（T3）、12h（T4）、24h（T5）和48h（T6）共6个亚组,每组8只;检测不同时间点大鼠血清S100β含量及脑含水量,并观察脑组织病理变化.结果 模型组和尼莫地平组的血清S100β蛋白含量及脑组织含水量在2h开始升高,24h达高峰,48h开始降低;与模型组相比,尼莫地平组的血清S100β蛋白含量各时间点均低于模型组（P＜0.05或P＜0.01）,脑含水量从T2～T5均低于模型组（P＜0.05或P＜0.01）;两组大鼠脑组织缺血再灌注24h均出现明显的病理变化,但尼莫地平组较模型组明显减轻.结论 尼莫地平能明显减轻脑损伤和脑水肿,对深低温停循环后的缺血大鼠脑组织有一定的保护作用.

Cerebral Protection Effect of Nimodipine during Deep Hypothermic Circulatory Arrest in Rats

Objective To investigate the protective effects and the mechanism of nimodipine on cerebral isehemia reperfusion injury during Deep Hypothermic Circulatory Arrest（DHCA）. Methods 96 male SD rats of DHCA model were randomly divided into the model group（DHCA） and nimodipine group（ DHCA ＋ Nimo- dipine） ,48 rats in each group. By two vessel occlusion combined with hypotension the rat models of cerebral ischemia reperfusion were established. According to the different time, each group was divided into ischemia reperfusion Oh （Tj）, 2h （T2）, 6h （T3）, 12h （T4）, 24h （Ts） and 48h （T6） consisted of 6 sub groups,8 rats in each group. The content of S100β in serum and brain ＇water content were measured at different time points. Results The content of S100β in serum and brain water content began to increase after ischemiareperfusion 2h in the model group and the nimodipine group, reached the peak after 24h,then began to decrease after 48h. The model group （ P 〈 0.05 or P 〈 O. 01 ）. content of S10013 in serum at each The brain water content from T2 to time point were lower than that in T5 in Nimodipine group were lower than that in the model group （ P 〈 0.05 or P 〈 0.01 ）. Two groups of rats brain tissue showed obvious patholog- ical changes after ischemia reperfusion 24h. But compared with the model group, the nimodipine group was sig- nificantly reduced. Conclusion Nimodipine can obviously alleviate brain injury and brain edema and it has certain protective effect on ischemic brain tissues of rats after deep hypothermic circulatory arrest.