WE measured the brain uptake index (BUI) for radio-labelled L-ornithin
e (ORN) in rats with acute hepatic encephalopathy (HE) induced by two
(onset stage) or three (comatous stage) administrations of a hepatotox
in-thioacetamide TAA). In the comatose group, an increase of the BUI t
o 275% of control was measured at 24 h post-treatment. In the onset gr
oup, the BUI for ORN increased gradually with time: it reached 220% of
control at 7 days post-treatment and 442% of control at 21 days post-
treatment. HE did not raise the BUI for a blood-brain barrier (BBB) no
n-penetrable amino acid L-aspartate (ASP), indicating that HE activate
s ORN transport but does not produce BBB leakage. ORN transport throug
h BBB was not increased in rats with hyperammonemia comparable to that
accompanying HE, but was induced without liver damage. Considering re
cent evidence that ORN acting intracerebrally ameliorates pathophysiol
ogical symptoms of HE, increased transport ORN across BBB should facil
itate HE therapy based on systemic administration of this amino acid.