摘要
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 glutamate and glutamate receptor in the secondary injury of spinal cord
ischemia reperfusion injury and its APV effects.Method:The model of ischemia and reperfusion
of spinal cord was created by the 60 min occlusion of the lunbar artery in 70 rabbits with the
weight of 2 25±0 25kg,the activity (Bmax,K D) of glutamate receptor (GluR) was measured by
the radioligand binding assay in the injured group and 2 amino 5 phosphono valerate(APV)
treated group during the 0 5～24h of ischemia decreased.Result:Bmax increased remarkably
at the beginning of reperfusion and reached to the peak at 2h of reperfusion and then decreased
gradually to the lowest level at 4h of reperfusion.K D continued to drop at 0.5h of
reperfusion,after that time,its change was the same as that of the Bmax.APV could improve the
activity of GluR during the early period of reperfusion,but there was no significant effect after 4h
of reperfusion.Conclusion:Glu involved in the secondary injury of spinal cord ischemia
reperfusion injury by its receptor.But the activity of GluR has different effects in the injury
progression.It is suggested that Glu excited toxicity is not the only reasons of the secondary
injury of spinal cord ischemia reperfusion.
出处
《中国脊柱脊髓杂志》
CAS
CSCD
1999年第4期212-215,共4页
Chinese Journal of Spine and Spinal Cord
关键词
谷氨酸受体
脊髓缺血损伤
再灌流
家兔
Glutamate receptor\ Spinal cord injury\
Ischemia and reperfusion\ Rabbit
