Zaki A E, Ede R J, Davis M, Williams R
Hepatology. 1984 May-Jun;4(3):359-63. doi: 10.1002/hep.1840040302.
Permeability of the blood brain barrier in relation to the development of hepatic encephalopathy was investigated in two animal models of acute hepatic failure, in one of which there was the potential for recovery (D-galactosamine-induced hepatitis). In both this and the hepatic devascularization model, there was an approximate 3-fold increase in the passive permeability of the blood brain barrier to inulin and sucrose. Transport of amino acids was also significantly affected, with approximate 30% increases in the brain uptake of phenylalanine, tyrosine and arginine and a 65% increase in uptake of leucine. These changes are attributed to the action of circulating toxic substances, some of which increase blood brain barrier permeability in normal animals.
在两种急性肝衰竭动物模型中研究了血脑屏障通透性与肝性脑病发展的关系，其中一种模型有恢复的可能（D-半乳糖胺诱导的肝炎）。在这种模型和肝去血管化模型中，血脑屏障对菊粉和蔗糖的被动通透性均增加了约3倍。氨基酸转运也受到显著影响，苯丙氨酸、酪氨酸和精氨酸的脑摄取量增加了约30%，亮氨酸摄取量增加了65%。这些变化归因于循环有毒物质的作用，其中一些物质会增加正常动物的血脑屏障通透性。
