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Increased brain quinolinic acid (QUIN) levels have been suggested to play a role in hepatic encephalopathy (HE). Previous brain tissue studies have been unable to confirm this hypothesis. Because QUIn is a potent NMDA-receptor agonist, it also is relevant to determine brain extracellular QUIN levels in HE. For this purpose, we assessed frontal neocortical extracellular QUIN levels by in vivo microdialysis in rats subjected to a portacaval shunt (PCS). We also evaluated the acute effects of altered L-tryptophan (L-TRP) availability on brain extracellular QUIN levels. The basal extracellular L-TRP levels were significantly (p &lt; .001) higher in the PCS rats than in the sham-operated controls. However, the QUIN level (p &lt; .05) and the QUIN to L-TRP ratio (p &lt; .01) were significantly lower in the PCS rats. Elevated L-TRP availability increased the QUIN levels to a similar degree in both sham and PCS rats. This study, in conjunction with our previous results, does thereby not support a major involvement of QUIN in the pathogenesis of HE.

Brain Extracellular Quinolinic Acid in Chronic Experimental Hepatic Encephalopathy as Assessed by In Vivo Microdialysis: Acute Effects of L-Tryptophan