脊髓缺血再灌注损伤后神经功能修复的实验研究

目的研究青紫兰兔脊髓缺血40min和再灌注4h脊髓组织兴奋性氨基酸（EAAs）和细胞内Ca

An experimental study of neuronal function restoration following ischemic reperfusion injury of spinal cord

Objective　To study the content varies of excitatory amino acids (EAAs)and intracellular calcium(［Ca2+］i)of spinal cord tissues from lumbar spinal cord in rabbits after 40 minutes of ischemia and 4 hours of reperfusion, and to observe the effects of the EAAs receptor antagonists ketamine on aforementioned targets.　 Methods　Thirty healthy rabbits were divided into 6 groups: sham-operation, 40 minutes of ischemia, 4 hours of reperfusion, 4 hours of reperfusion treatment with ketamine, MgSO4 and physiological saline groups. The contents of EAAs (glutamate and aspartate) and ［Ca2+］i were measured. In addition, the effects of ketamine and MgSO4 on aforementioned targets were observed in these rabbits. 　Results　 The results revealed that in group of 40 minutes after ischemia, the GLU and ASP contents of the EAAs transmitterswere decreased to (15.18±2.33) μmol/g， (9.99±0.69) μmol/g differently,and further to (13.75±2.58) μmol/g, (6.49±1.39) μmol/g after reperfusion. But after 40 minutes of ischemia, ［Ca2+］i was elevated to (221.2±4.27)μg/g, and further to (298.3±9.26) μg/g after the reperfusion, which were more significantly than that of ischemia and control groups. Ketamine could increase obviously the level of GLU and ASP to (21.51±5.42) μmol/g and (9.55±2.45) μmol/g, and decrease the ［Ca2+］i to (218.6±7.08) μg/g during the ischemia and reperfusion.　Conclusions　The study proves that the excitotoxicity of EAAs and the overload of calcium induced by EAAs play an important role in spinal cord ischemia-reperfusion injury. Ketamine demonstrates an effective restrained role to the injury mechanism and has a good prospect.