Abstract
Hepatic encephalopathy (HE) is a clinical condition resulting from either insufficient liver function or the construction of a shunt from the portal to the systemic circulation. As a result, several compounds known to be neurotoxic are no longer removed from the blood by the liver. Hepatic encephalopathy is characterized by increasing neurological impairment leading to coma (for review see Duffy and Plum, 1982). Although information is available from both clinical studies and from research using experimental animal modes of HE, there is still much that is unknown about the biochemical mechanisms involved in the pathogenesis of this disorder. Of the several toxic compounds increased in the blood and in brain tissue during the course of HE, the finding of an increased ammonia concentration has received the most attention (Butterworth et al., 1987).
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Fitzpatrick, S.M., Behar, K.L., Shulman, R.G. (1989). In Vivo NMR Spectroscopy Studies of Cerebral Metabolism in Rats after Portal-Caval Shunting.. In: Butterworth, R.F., Layrargues, G.P. (eds) Hepatic Encephalopathy. Experimental Biology and Medicine, vol 22. Humana Press. https://doi.org/10.1007/978-1-4612-4506-3_12
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DOI: https://doi.org/10.1007/978-1-4612-4506-3_12
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