镁预处理对兔全脑缺血神经保护作用的实验研究  

Experimental Research of Neuroprotective Effect of Magnesium Sulfate Preconditioning on Global Ischemia in Rabbits

作　　者：欧册华[1] 张毅[2] 李惠芳[2] 

机构地区：[1]泸州医学院附属医院麻醉科,四川泸州646000 [2]昆明医学院第一附属医院麻醉科

出　　处：《四川动物》2009年第3期437-439,共3页Sichuan Journal of Zoology

摘　　要：目的探讨硫酸镁预处理对兔全脑缺血神经保护作用及其机制。方法45只兔随机分为3组:对照组(n=15)、缺血组(n=15)和镁预处理组(n=15)。阻断血管,诱导全脑缺血,缺血时间为6 min。测定缺血再灌注30 min兔海马谷氨酸、天冬氨酸、γ-氨基丁酸和甘氨酸含量。检测缺血再灌注3 d海马CA1区神经元密度和凋亡神经元密度。结果(1)镁预处理组海马天冬氨酸和甘氨酸显著低于缺血组(P<0.01),而γ-氨基丁酸含量显著高于缺血组(P<0.05);(2)镁预处理组正常神经元密度显著高于缺血组(P<0.01),缺血神经元密度显著低于缺血组(P<0.01);(3)镁预处理组凋亡神经元密度显著低于缺血组(P<0.01)。结论(1)硫酸镁预处理对兔全脑缺血有神经保护作用;(2)该保护作用的机制可能有:1)抑制兔全脑缺血再灌注30 min海马天冬氨酸和甘氨酸的过度释放以及抑制γ-氨基丁酸的耗竭;2)抑制兔全脑缺血再灌注3 d海马CA1区神经元凋亡。Objective To explore the neuroprotective effect of magnesium sulfate preconditioning on global ischemia in rabbits. Methods 45 rabbits were divided randomly into three groups ： control group （ n = 15 ）, ischemie group （ n = 15 ） and magnesium preconditioning group （ n = 15 ）. Global ischemia was produced by occlusion of four vessels for 6 min. Glutamate （Glu）, aspartic acid （ASP）, gamma-aminobutyrie acid （GABA） , and glycine （Gly） levels in the hippocampus were measured 30 min after reperfusion. The densities of neurons and apoptosis neurons in the hippoeampal CA1 field were measured 3 days after reperfusion. Results （ 1 ） The content of ASP and Gly in the magnesium preconditioning group was significantly lower than that of isehemic group （ P 〈 0.01 ）. The content of GABA in the magnesium preconditioning group was significantly higher than that of isehemic group （P 〈 0.05 ）. （2） The density of normal neurons in the magnesium preconditioning group was significantly higher than that of isehemic group （ P 〈 0.01 ） ; The density of isehemie neurons was significantly lower than that of isehemic group （P 〈 0.01 ）. （3） The density of apoptosis neurons in the magnesium preconditioning group was significantly lower than that of isehemie group （ P 〈 0.01 ）. Conclusion （ 1 ） Magnesium sulfate could have a neuroprotective effect on global ischemia in rabbits. （2） The neuroprotective mechanism could include： 1 ） inhibiting the massive release of ASP and Gly, and inhibiting the exhaust of GABA in the hippoeampus 30 min after reperfusion. 2 ） inhibiting neuronal apoptosis in the hippoeampal CA1 field 3 days after reperfusion.

关 键 词：镁离子 全脑缺血 神经保护 预处理 

分 类 号：R743[医药卫生—神经病学与精神病学]