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Schafer在1982年提出的肝性脑病发病机理的GABA假说已在多方面得到实验支持。但肝损害时GABA进入脑组织是否增加至今未见直接报导。我们以尾静脉注射~3H-GABA进行同位素示踪,并用醋酸纤维素薄膜电泳将~3H-GABA与其代谢物分离。测定D-氨基半乳糖诱发肝性脑病的小鼠血和脑中放射性GABA(S/T%,B/T%)以及它在总非挥发性放射性物质中的构成比(S~3H-GABA%,B~3H-GABA%)。所得结果表明,实验性肝性脑病小鼠的S/T%,B/T%,S~3H-GA-BA%及B~3H-GABA%都明显高于正常小鼠,即肝性脑病时,脑从血中摄取GABA增加,推测是由于血脑屏障对GABA的通透性发生改变所致
The GABA hypothesis that Schafer proposed in 1982 for the pathogenesis of hepatic encephalopathy has been experimentally supported in many ways. However, there is no direct report on whether GABA enters the brain tissue during liver damage. We performed isotope labeling with ~ 3H-GABA in the tail vein and ~ 3H-GABA was separated from its metabolites using cellulose acetate membrane electrophoresis. The ratio of radioactive GABA (S / T%, B / T%) in blood and brain of D-galactosamine-induced hepatic encephalopathy and its proportion in total non-volatile radioactive material , B ~ 3H-GABA%). The results showed that the experimental hepatic encephalopathy in mice S / T%, B / T%, S ~ 3H-GA-BA% and B ~ 3H-GABA% were significantly higher than normal mice, hepatic encephalopathy , Increased brain uptake of GABA from the blood, presumably due to altered permeability of GABA by the blood-brain barrier