Titlebook: Hepatic Encephalopathy in Chronic Liver Failure; Livio Capocaccia,Joseph E. Fischer,Filippo Rossi-F Book 1984 Plenum Press, New York 1984

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Role of Synergism in the Pathogenesis of Hepatic Encephalopathy, and that other endogenous abnormalities augment the toxicity of these substances (Figure 1). Four of the substances that accumulate during hepatic failure have been shown unequivocally to cause coma in experimental animals. These are ammonia, mercaptans, fatty acids, and phenols. The role of ammon

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γ-Aminobutyric Acid Receptors in Experimental Hepatic Encephalopathyblood, in cerebrospinal fluid or in brain with the aim of recognizing the primary factors leading to the central nervous system (CNS) dysfunction of coma. Because of the numerous metabolic abnormalities found in this pathology a congeries of theories has been generated, but none of these is so fully

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A Possible Role for Excitatory Neurotoxic Amino Acids in the Pathogenesis of Hepatic Encephalopathyral neurological and psychiatric disorders.. However, relatively little information is available on the role of glutamic acid (GLU), the prototype of acidic excitatory amino acids, in the pathogenesis of hepatic encephalopathy..

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Alterations of Plasma and Brain Tryptophan in Hepatic Encephalopathy: A Study in Humans and in Experchronic liver failure. In a group of 149 patients with liver cirrhosis, it was shown that plasma free tryptophan (the amino acid not bound to albumin) significantly rose when liver function was impaired. This increase was well correlated to the grade of hepatic encephalopathy. The ratio free tryptop

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New Methods for the Determination of Serum and Breath Mercaptans and Its Application in Liver Cirrhos being one of the endogenous factors responsible for hepatic coma.. The reports in literature on breath. and serum or blood mercaptans. are highly conflicting. This is probably due to differences in assay and to technical difficulties to measure mercaptans in a reproducible way. The reports on seru

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Hepatic Encephalopathy is Associated with Decreased Numbers of Receptors for Excitatory Aminoacid Nes which are associated with liver failure and which could conceivably contribute to the mediation of this syndrome. Several observations have suggested that in liver failure impairment of cerebral neurotransmission may occur. In the “false neurotransmitter hypothesis” of the pathogenesis of HE propo