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目的：探讨谷氨酸（Ｇｌｕ）及其受体（ＧｌｕＲ）在脊髓缺血过程中的量变特征在继发损伤中的作用及２氨基膦酸基戊酸（ＡＰＶ）的治疗作用。方法：选用体重２～２５ｋｇ的日本大耳白家兔７０只，用腰动脉分支阻断法建立脊髓缺血模型，用放射配基结合分析法检测脊髓缺血损伤后０５～２４ｈ期间及在缺血６０ｍｉｎ时用ＡＰＶ处理后脊髓神经细胞膜的ＧｌｕＲ活性（Ｂｍａｘ，ＫＤ）。结果：缺血６０ｍｉｎ后ＧｌｕＲ的最大结合量降低，亲和力升高，开始再灌流后最大结合量迅速升高，至２ｈ到达高峰，之后迅速下降，至再灌流４ｈ降至最低，此后缓慢回升，而亲和力在再灌流０５ｈ时继续升高，然后下降，再灌流２ｈ降至最低，此后趋势与最大结合量变化相反。ＡＰＶ在再流灌早期使受体活性增高，再灌流４ｈ后无显著性差异。结论：Ｇｌｕ通过其受体中介参与了脊髓缺血再灌流损伤，但在缺血再灌流过程中ＧｌｕＲ活性的变化可能具有不同的作用效应，同时也说明脊髓继发性损伤机制单以Ｇｌｕ兴奋性损伤是解释不了的。
Objective: To investigate the role of glutamine (Glu) and its receptor (GluR) in secondary spinal cord injury following spinal cord ischemia and the therapeutic effect of 2aminophosphonopentanoic acid (APV). Methods: Seventy rabbits of Japanese white-ear rabbits weighing 2- 2.5 kg were used to establish the model of spinal cord ischemia with branch block of lumbar artery. Radioligand binding assay was used to detect the spinal cord injury from 05 to 24h Glucose binding activity (Bmax, KD) of neurons in spinal cord after treatment with APV for 60min after ischemia. Results: After 60min of ischemia, the maximum binding capacity of GluR decreased and the affinity increased. The maximum binding capacity increased rapidly after reperfusion and peaked at 2h, then decreased rapidly to a minimum after 4h of reperfusion, Affinity in 05h reperfusion continue to rise, then decreased, 2h reperfusion down to a minimum, since the trend and the maximum combination of changes in the opposite. In the early stage of reperfusion, APV increased the activity of receptor, and there was no significant difference after reperfusion for 4 hours. CONCLUSION: Glu participates in spinal cord ischemia-reperfusion injury through its receptor mediator, but GluR activity may have different effects during ischemia-reperfusion. It also shows that the mechanism of secondary spinal cord injury is Glu excitability Damage can not be explained.