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γ 氨基丁酸受体系统中α ,β亚基与配体结合时均产生相同的效果 ,使脑细胞静息膜电位增大 ,表现为抑制作用。肝性脑病患者血液中存在内源性BZ样物质BZD及抑制BZD与GABA BZ受体结合的神经肽DBI。患肝性脑病时BZD水平升高 ,而DBI水平降低 ,血氨通过星状细胞分泌神经类固醇兴奋GA BA BZ受体复合物产生脑细胞的抑制从而阐明了肝性脑病患者脑细胞功能紊乱的发生机制。
γ-aminobutyric acid receptor system, α and β subunits and ligand binding have the same effect, the resting membrane potential of brain cells increased, showed inhibition. In the blood of patients with hepatic encephalopathy there is an endogenous BZ-like substance BZD and a neuropeptide DBI that inhibits the binding of BZD to the GABA BZ receptor. In patients with hepatic encephalopathy, the level of BZD is elevated and the level of DBI is decreased. Blood ammonia, through the secretion of neurosteroids by stellate cells, stimulates the inhibition of brain cells by the GA BA BZ receptor complex, thereby clarifying the occurrence of brain cell dysfunction in patients with hepatic encephalopathy mechanism.