Abstract
Hepatic encephalopathy precipitated by hepatocellular failure has been extensively studied, but the neural mechanisms that mediate this syndrome remain unknown1–3. It is still uncertain whether hepatic encephalopathy is due to diminished hepatic synthesis of a substance necessary for normal brain function or diminished hepatic metabolism of a substance which can induce neural inhibition. Two observations tend to favour the second of these possibilities. One is the clinical observation that therapeutic manoeuvres which reduce the interaction between nitrogenous substances and the enteric bacterial flora are often followed by the amelioration of hepatic encephalopathy in patients with cirrhosis1. The other is the result of carefully conducted experiments in which normal and liverless rats were cross-circulated and the E.E.G. monitored; brain function of liverless rats improved more rapidly when their aortic blood was infused into the portal vein rather than the jugular vein of normal rats4.
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Jones, E.A. (1985). Recent trends in studies of the pathogenesis of hepatic encephalopathy. In: Bianchi, L., Gerok, W., Popper, H. (eds) Trends in Hepatology. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-4904-1_12
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DOI: https://doi.org/10.1007/978-94-009-4904-1_12
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-8672-1
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