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目的目前,大血管手术和复杂先心病术中深低温停循环下神经系统的保护仍有较大提升空间。为了探寻神经保护新的思路,我们对不同温度下停循环的大鼠海马组织进行了损伤评估。方法20只雄性SD大鼠随机分为4组:深低温停循环(15~20℃),中低温停循环(20~25℃),浅低温停循环(25~30℃)和假手术组。术后对大鼠海马组织进行了病理评估,对神经元树突中的微管相关蛋白2(microtubule-associated protein 2,MAP2)的表达,进行了实时定量PCR和蛋白免疫印迹分析。血浆中MAP2和S100β的含量也通过ELISA法进行了测定。结果与假手术相比,各组低温停循环大鼠的海马神经元的树突微管和线粒体嵴均有溶解。与假手术组相比,浅低温停循环组海马组织中MAP2的mRNA表达上调,MAP2蛋白组间无差异。各组血浆S100β含量并无统计学差异,而与假手术组相比,浅低温停循环组的血浆MAP2升高。结论低温停循环后,神经元的树突受损,微管溶解,其构成蛋白MAP2释放到血液。促进MAP2生成,减少MAP2的损失可能是一种有效的神经保护策略。
Objective Currently, there is still room for improvement in the protection of the nervous system under deep hypothermic circulatory arrest in major vascular surgery and complicated congenital heart disease. In order to find out a new way of neuroprotection, we evaluated the damage of hippocampus in rats with circulatory arrest at different temperatures. Methods Twenty male Sprague-Dawley rats were randomly divided into 4 groups: deep hypothermic circulatory arrest (15-20 ℃), hypothermic circulatory arrest (20-25 ℃), mild hypothermic circulatory arrest (25-30 ℃), and sham operation group. The histopathological evaluation of the hippocampus of rats was performed after surgery. The expression of microtubule-associated protein 2 (MAP2) in dendrites of neurons was analyzed by real-time PCR and Western blotting. The levels of MAP2 and S100β in plasma were also determined by ELISA. Results Compared with sham operation, the dendritic microtubules and mitochondrial crista of hippocampal neurons in each group of hypothermic circulatory arrest rats were dissolved. Compared with the sham operation group, MAP2 mRNA expression was up-regulated in the hippocampus of the light hypothermic circulatory arrest group, but no difference was found between the MAP2 protein groups. There was no significant difference in plasma levels of S100βin each group, but plasma MAP2 in mild hypothermic circulatory arrest group was higher than that in sham operation group. Conclusions After hypothermic circulatory arrest, the dendrites of neurons are damaged and the microtubules are dissolved, releasing its constituent protein MAP2 to the bloodstream. Promoting MAP2 production and reducing MAP2 loss may be an effective neuroprotective strategy.