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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References
Behar, K.L., Rothman, D.L., Fitzpatrick, S.M., Hetherington, H.P., and Shulman, R.G. (1987). Combined 1H and 31P NMR studies of the rat brain in vivo: Effects of altered intracellular pH on metabolism. In: Physiological NMR Spectroscopy: From Isolated Cells to Man (S. Cohen, ed.), pp. 81–88. New York Academy of Science, New York.
Behar, K.L., den Hollander, J.A., Stromski, M.E., Ogino, T., Shulman, R.G., Petroff, O.A.C. and Prichard, J.W. (1983). High resolution 1H NMR study of cerebral hypoxia in vivo. Proc. Natl. Acad. Sci. USA 81, 4945–4948.
Behar, K.L., den Hollander, J.A., Petroff, O.A.C, Hetherington, H.P., Prichard, J.W. and Shulman, R.G. (1985). Effect of hypoglycemic encephalopathy upon amino acids, high energy phosphates, and pH in the rat brain in vivo: detection by sequential 1H and 31P NMR spectroscopy. J. Neurochem. 44, 1045–1055.
Bendall, M.R., and Gordon, R.D. (1983). Depth and refocusing pulses designed for multipulse NMR with surface coils. J. Magn. Reson. 53, 365385.
Butterworth, R.F., Giguere, J.F., Michaud, J., Lavoie, J. and Pomier Layrargues, G. (1987). Ammonia: key factor in the pathogenesis of hepatic encephalopathy. Neurochem. Pathol. 6, 1–12.
Butterworth, R.F., Girard, G., and Giguere, J.F. (1988). Regional differences in the capacity for ammonia removal by brain following portocaval anastomosis. J. Neurochem. 51, 486–490.
Cooper, A.J.L. and Plum, F. (1987). Biochemistry and physiology of brain ammonia. Physiol. Rev. 67, 440–519.
Duffy, T.E. and Plum, F. (1982). Hepatic encephalopathy. In: The Liver: Biology and Pathobiology (I. Arias, H. Popper, D. Schacter and D.A. Shafritz, eds.), pp. 693–751. Raven Press, New York.
Fitzpatrick, S.M., Hetherington, H.P., Behar, K.L. and Shulman, R.G. (1989). Effects of acute hyperammonemia on cerebral amino acid metabolism and pH in vitro, measured by 1H and 31P Nuclear Magnetic Resonance. J. Neurochem. 52 (in press).
Hetherington, H.P. (1988). The design and application of multipulse NMR techniques to in vivo 1H NMR. Ph.D. thesis, Yale Univ., New Haven, CT.
Hetherington, H.P. and Rothman, D.L. (1985). Phase cycling of composite refocusing pulses to eliminate dispersive refocusing magnetization. J. Magn. Reson. 65, 348–354.
Hindfelt, B., Plum, F. and Duffy, T.E. (1977). Effect of acute ammonia intoxication on cerebral metabolism in rats with portocaval shunts. J. Clin. Invest. 59, 386–396.
Hore, P.J. (1983). Solvent suppression in Fourier transform nuclear magnetic resonance. J. Magn. Reson. 55, 386–396.
McKhann, G.M. and Tower, D.B. (1961). Ammonia toxicity and cerebral oxidative metabolism. Am. J. Physiol. 200, 420–424.
Patlack, C.S. and Pettigrew, K.D. (1976). A method to obtain infusion schedules for prescribed blood concentration time courses. J. Appl. Physiol. 40, 458–463.
Petroff, O.A.C., Prichard, J.W., Behar, K.L., Alger, J.R., den Hollander, J.A. and Shulman, R.G. (1985). Cerebral intracellular pH by 31P nuclear magnetic resonance spectroscopy. Neurology 35, 781–788.
Petroff, O.A.C., Prichard, J.W., Behar, K.L., Alger, J.R. and Shulman, R.G. (1984). In vivo phosphorus nuclear magnetic resonance spectroscopy in status epilecticus. Ann. Neurol. 16, 169–177.
Plateau, P. and Gueron, M. (1982). Exchangeable proton NMR without base-line distortion, using new strong-pulse sequences. J. Am. Chem. Soc. 104, 7310–7311.
Zieve, L. (1981). The mechanism of hepatic coma. Hepatology 1, 360–365.
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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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