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目的:探讨海马微环境内异常谷氨酸与局部脑血流(regional cerebral blood flow,rCBF)互动变化及其可能机制。方法:单泵等速微灌流系统分别行树鼩海马高、中、低谷氨酸微灌流4 h,通过激光多普勒血同时NM-DA-NR1表达增加流计测量海马CA1区rCBF含量;并用免疫组化观察海马CA1区血管内皮细胞NMDA-NR1表达。微灌流谷氨酸溶液后原位灌流其受体拮抗剂MK-801,并观测上述指标改变。结果:树鼩微环境内随着谷氨酸的增加海马rCBF逐渐降低(P<0.01),其中高浓度谷氨酸微灌流后的rCBF(PU)最低(6.9±0.3,P<0.01)同时NMDA-NR1表达增加(P<0.01),使用Glu受体NMDA拮抗剂MK-801后可显着升高rCBF,同时可降低NM-DA-NR1表达(P<0.01)。结论:海马神经元微环境中Glu增多时,可诱导局部脑血管内皮细胞损伤继而可能是诱发海马神经元损伤的原因之一。
Objective: To investigate the interaction between abnormal glutamate and regional cerebral blood flow (rCBF) in hippocampal microenvironment and its possible mechanism. Methods: Single-pump isokinetic microperfusion system was used to detect the content of rCBF in the hippocampal CA1 region by high, medium and low glutamate microdialysis in the hippocampus for 4 h. Immunohistochemistry was used to observe the expression of NMDA-NR1 in vascular endothelial cells of hippocampal CA1 area. Microperfusion perfusion of glutamate solution in situ perfusion of its receptor antagonist MK-801, and observed the above indicators change. Results: The rCBF of hippocampus decreased gradually with the increase of glutamate (P <0.01), and the lowest of rCBF (PU) after high concentration of glutamate microperfusion (6.9 ± 0.3, P <0.01) (P <0.01). The MK-801 with Glu receptor NMDA antagonist increased rCBF and decreased the expression of NM-DA-NR1 (P <0.01). Conclusion: The increase of Glu in the hippocampal neuron microenvironment may induce the injury of local cerebrovascular endothelial cells, which may be one of the reasons of inducing hippocampal neuron injury.