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Do Benzodiazepine Ligands Contribute to Hepatic Encephalopathy?

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Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 341))

Abstract

Since 1985 (1,2) evidence has been accumulating which indicates that benzodiazepine (BZ) ligands with agonist properties may contribute to the pathogenesis of hepatic encephalopathy (HE) by potentiating the neuroinhibitory action of GABA. The status of this hypothesis in 1989 was reviewed at the International Symposium on Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity held in Valencia (3). The purpose of this paper is to discuss developments in this field that have occurred since that review. These developments have occurred on two main fronts: (i) Detection, characterization and purification of BZ receptor ligands in tissue of animals and humans with HE; and (ii) Evaluation of the effects of BZ receptor ligands on HE in animal models and humans. The new findings are discussed after summarizing the main points covered by the review at the Valencia meeting (3).

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Jones, E.A., Basile, A.S., Yurdaydin, C., Skolnich, P. (1993). Do Benzodiazepine Ligands Contribute to Hepatic Encephalopathy?. In: Grisolía, S., Felipo, V. (eds) Cirrhosis, Hyperammonemia, and Hepatic Encephalopathy. Advances in Experimental Medicine and Biology, vol 341. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2484-7_6

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  • DOI: https://doi.org/10.1007/978-1-4615-2484-7_6

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