Ischemia-reperfusion injury following hepatic portal occlusion increases brain excitatory amino acids and NMDAR mRNA expression in rats

AIM: To explore the changes of excitatory amino acids and N-methyl-D-aspartate receptor (NMDAR) in brain undergoing ischemia-reperfusion injury following hepatic portal occlusion (HPO) in vivo.METHODS: The electrolytes and pH of portal vein blood,the content of Glu and Asp in brain,and the expression of NMDAR mRNA were studied with blood-gas analysis,HPLC and semi-quantitative RT-PCR method in two groups(HPO or sham),respectively.Three time points(6 h,12 h and 24h after reperfusion) were included.RESULTS: HPLC measure showed that the content of cortex Glu and Asp in group HPO elevated significantly after reperfusion compared with sham group, the peaks were at 6 h and 24 h ［Glu:(349±145) μg·g^-1wt,(456±203) μg·g^-1wt vs (238±24) μg·g^-1wt,(225±59) μg·g^-1wt;Asp:(134±50) μg·g^-1wt,(166±50) μg·g^-1wt vs (99±24) μg·g^-1wt,(71±20) μg·g^-1wt］.Moreover,semi-quantitative RT-PCR analysis discovered that the expression of NMDAR mRNA increased significantly ,the subunit NR1 mRNA was higher in reperfusion 6 h and last to 12 h（1.63±0.06 vs 1.18±0.05;1.73±0.06 vs 1.17±0.03）,the peak of NR2B mRNA was in 12 h (1.75±0.04 vs 1.18±0.05) ,but they did not further increase after reperfusion for 24 h.CONCLUSION: HPO increases the content of Glu and Asp and the expression of NMDAR in brain cortex.The Glu-NMDAR pathway plays a role in the mechanism for the brain injury after HPO.The products of IR injury might be the key factor to cause EAAs acumulation in synapse space.