Ischemia-reperfusion injury following hepatic portal occlusion increases brain excitatory amino acids and NMDAR mRNA expression in rats / 中国病理生理杂志

ABSTRACT

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) ?g?g-1wt,(456?203) ?g?g-1wt vs (238?24) ?g?g-1wt,(225?59) ?g?g-1wt;Asp(134?50) ?g?g-1wt,(166?50) ?g?g-1wt vs (99?24) ?g?g-1wt,(71?20) ?g?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.