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The Use of Cultured Astrocytes in the Study of Hepatic Encephalopathy

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Part of the book series: Experimental Biology and Medicine ((EBAM,volume 22))

Abstract

Considerable data implicates astrocytes in the pathogenesis of hepatic encephalopathy (HE). The Alzheimer type II astrocyte change constitutes the histopathologic hallmark in man and experimental animals with portal systemic encephalopathy (for reviews, see Norenberg, 1981, 1987). Ammonia, the chief toxin implicated in the pathogenesis of HE also causes similar astrocytic changes. Additionally, the detoxification of ammonia in brain occurs through the action of glutamine synthetase, an enzyme which in brain is exclusively localized in astrocytes (Norenberg and Martinez-Hernandez, 1979). Other implicated toxins, such as short-chain fatty acids also appear to be predominantly metabolized in astrocytes (Cremer, 1975). Finally, fulminant hepatic failure leads to the development of cerebral edema, a condition caused by water accumulation in astrocytes (Traber et al., 1987).

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Norenberg, M.D. (1989). The Use of Cultured Astrocytes in the Study of Hepatic Encephalopathy. 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_15

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  • DOI: https://doi.org/10.1007/978-1-4612-4506-3_15

  • Publisher Name: Humana Press

  • Print ISBN: 978-1-4612-8851-0

  • Online ISBN: 978-1-4612-4506-3

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