不同脑温状态银杏叶提取物对大鼠脑缺血组织兴奋性氨基酸的影响

The Effects of Ginkgo Biloba Extract under Different Cerebral Temperature on the Excitatory Amino Acids Concentration in Focal Cerebral Ischemia of Rat

目的：探讨不同脑温状态下银杏叶提取物（GBE）对大鼠脑缺血组织谷氨酸（Glu）、天门冬氨酸（Asp）的影响。方法：建立大鼠大脑中动脉缺血再灌注模型，诱导目标脑温，测定各组脑缺血组织Glu、Asp含量。结果：（1）与常温假手术组比较，常温脑缺血对照组及常温银杏叶组Glu、Asp水平均显著增高（P〈0．001）。（2）与常温脑缺血对照组比较，常温银杏叶组及亚低温脑缺血组Glu、Asp水平均显著降低（P〈0．001）。（3）与常温银杏叶组比较。轻度高温银杏叶组Glu、Asp水平均显著增高（P〈0．001）；亚低温脑缺血组及亚低温银杏叶组Glu、Asp水平均显著降低（P〈0．01-0．001）.（4）与亚低温脑缺血组比较，亚低温银杏叶组Glu、Asp水平差异均无统计学意义（P〉0．05）。结论：（1）脑缺血时，GBE降低Glu“兴奋毒性”的作用受不同脑温的影响。常温状态下，GBE有降低Glu“兴奋毒性”的作用，从而对脑缺血有保护作用；轻度高温状态下，GBE无此作用；而亚低温状态下，GBE的作用增强，从而增强对脑缺血的保护作用。（2）亚低温和GBE联合干预，降低Glu“兴奋毒性”，增强对脑缺血的保护作用，可能不是单一因素的作用，而是亚低温作用为主，两种干预因素共同协同作用的结果。

Objective ： To study the effect of Ginkgo biloba extract （GBE） on the concentration of Glu and Asp in rat ischemia brain under different cerebral temperature. Methods ： The model of rat middle cerebral artery ischemia reperfusion was established, induced to target cerebral temperature, then detected the concentration of Glu and Asp in variant ischemia brain group of high temperature, normal temperature, and subhypothermia. Results ： （1） Compared with sham operated group in normal temperature, the concentration of Glu and Asp were predominantly increased in cerebral ischemia control group and GBE group （P〈0.001）. （2） Compared with cerebral ischemia control group in normal temperature, the concentration of Glu and Asp were decreased in GBE group under normal temperature and cerebral isehemia group under subhypothermia （P〈0.001）. （3） Compared with GBE group under normal temperature, Glu and Asp concentration were notably increased （P〈0.001） in GBE group under mild high temperature while notably decreased （P〈0.01-0.001） in cerebral ischemia group and GBE group under subhypothermia. （4） Compared with cerebral ischemia group in subhypothermia, Glu and Asp concentration have no distinct diversity （P〉0.05） in GBE group under subhypothermia. Conclusion： （1） The cerebral temperature may affect GBE decreasing the exitotoxicity of Glu in cerebral ischemia. The GBE can decrease the exitotoxieity of Glu under normal temperature; those effect may be attenuated at mild hyperthermia while enhanced under subhypothermia, then enhance neuroprotection of GBE. （2） It suggests that the effect of decreasing the exitotoxicity of Glu, when subhypothermia combined with GBE, isn＇t the result of either subhypothermia or GBE intervention factor, but the main effect of suhhypothermia and cooperation of both.