硫酸镁和低分子肝素联合应用对海马迟发性神经元坏死的保护作用  

Protective effects of magnesium sulfate and low molecule heparin on ischemic reperfusion-induced hippocampal delayed neuronal death

作　　者：谷新医[1] 乔香兰[2] 王复新[2] 

机构地区：[1]长春市吉林大学中日联谊医院神经内科,130081 [2]黑龙江省佳木斯大学第一附属医院神经内科

出　　处：《中国局解手术学杂志》2003年第1期1-3,共3页

摘　　要：目的 研究硫酸镁和低分子肝素在短暂局灶性脑缺血再灌注后海马迟发性神经元坏死中的保护作用。方法新西兰大白兔夹闭单侧颈总动脉制成模型,缺血30 min再灌注72 h后通过HE染色进行组织观察,同时检测血清中IL-8的含量,探讨硫酸镁和低分子肝素对保护脑的作用机制。结果 硫酸镁联合低分子肝素治疗组迟发性神经元坏死程度显著低于盐水治疗组,低分子肝素能降低缺血再灌注后血清中的IL-8含量。结论IL-8做为一种急性炎症的趋化因子,在脑缺血时升高,可作为脑缺血炎症期或再灌注损伤重要的观察指标之一。硫酸镁没有抗炎作用,单用硫酸镁或低分子肝素的治疗效果,没有联合应用的治疗效果显著。Objective To study the role of magnesium sulfate and low molecular heparin (LMH) in hippocampal delayed neuronal death (DND)after transient local ischemic-reperfusion. Methods Ischemic-feperfusion model was made by clamping the common carotid artery of one side for 30 min and then reperfused for 72 h. Sections of hippocampus were staind by HE and studied. Serum IL-8 was determined by ELBA. Results The severity of neuronal damage in magnesium sulfate and LMH treated groups was significantly lower than that of saline treated group. LMH could decrese the serum content of IL- 8 after ischemic reperfusion. Conclusion IL- 8 can be an inflammatory factor during the ischemic and reperfu-sion injury. Magnesium sulfate has no anti-inflammation function. Administration of magnesium sulfate and LMH may exert protective effect on DND.

关 键 词：硫酸镁 低分子肝素 联合应用 海马 脑缺血 迟发性神经元坏死 保护作用 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R973.2[医药卫生—临床医学]