Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

Abstract

Taurine (Tau), an amino acid that abounds in brain, has been implicated in inhibitory neuromodulation and osmoregulation, the latter function being manifested by Tau release along with osmotically obligated water in response to brain tissue edema. A previous study (Hilgier and Olson: J. Neurochem. 62:197–204, 1994) had shown that simple hyperammonemia (HA) induced in rats by daily administration of ammonium acetate resulted in a decrease of both tissue specific gravity indicative of edema and Tau content, in basal ganglia (BG) but not in cerebral cortex (CC). By contrast, rats with hepatic encephalopathy (HE) following administration of a hepatotoxin, thioacetamide, were characterized by CC edema and an increased Tau content in both BG and CC. In the present study, we tested the following parameters that may potentially have affected Tau distribution in the two models: a) spontaneous, and stimulated (hypoosmolarity‐induced) release of loaded [3H] Tau in vitro from CC and BG slices; b) blood Tau content; and c) uptake of [14C] Tau in vivo from blood to brain corrected for [3H] water passage—the so‐called brain uptake index (BUI). The two edema‐affected structures: BG in the HA model and CC in the HE model, showed increased spontaneous Tau release. Edema‐associated spontaneous release of Tau may favor inhibitory neurotransmission contributing to the pathomechanism of HA or HE. Stimulated release, reflecting the ability of the tissue to reduce water content, was decreased in the BG from HA rats, in agreement with the postulated role of Tau in osmoregulation. Stimulated release was unchanged in CC of HE rats. Neither spontaneous nor stimulated release of Tau were affected in CC of HA rats or in BG of HE rats. HE, but not HA, was associated with elevated blood content and increased BUI for TAU, which in combination, contributed to the increase of Tau content in CC. The latter phenomenon adds to the list of metabolic changes distinguishing simple HA from toxic liver damage, reemphasizing the crucial role of factors other than ammonia in the pathomechanism of HE. © 1996 Wiley‐Liss, Inc.

Astroglial NMDA receptors inhibit expression of Kir4.1 channels in glutamate-overexposed astrocytes in vitro and in the brain of rats with acute liver failure

“…As repeatedly described in previous reports, this model faithfully reproduces basic symptoms of acuteto-subacute HE, including glutamatergic dysfunction and brain oedema (Hilgier et al, 1996;Rama Rao et al, 2010). The animals were sacrificed with carbon dioxide 72 h after the 1st TAA administration.…”

Intracerebral Administration of S-Adenosylhomocysteine or S-Adenosylmethionine Attenuates the Increases in the Cortical Extracellular Levels of Dimethylarginines Without Affecting cGMP Level in Rats with Acute Liver Failure

“…injections of thioacetamide (TAA) (300 mg/kg b.w.) at 24-h intervals (Hilgier and Olson 1994; Hilgier et al 1996) and sacrificed 24 h after third injection. Control rats received sodium saline solution (0.9 % NaCl).…”

The Na–K–Cl cotransporter in the brain edema of acute liver failure

“…This model has been established relative to the clinical status, liver function, and brain edema development [27][28][29][30]. Additionally, rats treated with TAA do not show impairment in blood-brain barrier integrity as assessed by the Evens-blue extravasation method (unpublished observations).…”