MK-801在脊髓缺血再灌注损伤中的作用

目的 研究大鼠脊髓缺血40min和再灌注4h脊髓组织兴奋性氨基酸(EAA)和细胞内Ca^2 ([Ca^2 ]i)的含量变化，及应用地卓西平马来酸盐(MK-801)对上述指标的影响。方法 SD大鼠40只，随机分为假手术组、缺血40min组、再灌注4h组、MK-801治疗组(n=10)。测定各组脊髓组织中谷氨酸(Glu)和[Ca^2 ]i含量，同时观察MK-801对上述指标的影响．结果 缺血40min组Glu含量明显降低，再灌注4h组Glu含量降低更明显；[Ca^2 ]i的含量在缺血40min组时有所升高，再灌注4h组则明显升高，MK-801组能显著升高Glu含量和降低[Ca^2 ]i的含量．结论 EAA的兴奋性神经毒性在脊髓缺血再灌注中发挥着重要的作用，MK-801对该神经毒性有明显的抑制作用。

Effects of MK-801 on Ischemic Reperfusion Injury of Spinal Cord in Rats

Objective To study the excitatory amino acids(EAA) and intracellular calcium content in spinal cord tissues in SD rats after 40 minutes of ischemia and 4 hours of reperfusion, and to observe the effects of the EAA receptor antagonists MK-801 on these index. Methods Forty SD rats were divided into 4 groups: sham-opertion, 40 minutes of ischemia, 4 hours of reperfusion, 4 hours of reperfusion with MK-801 intervention. The contents of EAA(glutamic,Glu) and [Ca+{2+}]i were measured. {Results} In group of 40 minutes ischemia, the Glu contents decreased and further decreased after reperfusion. But after 40 minutes ischemia,[Ca+{2+}]i was elevated and further elevated after the reperfusion. MK-801 can increase obviously the level of Glu, and decrease the level of [Ca+{2+}]i during the ischemia and reperfusion. Conclusion This study proves that the EAA and the overload of calcium induced by EAA play an important role in spinal cord ischemia-reperfusion injury. MK-801 demonstrates an effective protective role to prevent ischemic reperfusion injury of spinal cord.