SOME ASPECTS OF THE NITROGEN METABOLISM OF LIVER TISSUE FROM RATS IN HEMORRHAGIC SHOCK

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Abstract
Blood ammonia is sharply increased in rats in hemorrhagic shock, but not to toxic levels. The free ammonia of liver tissue is also increased slightly, but is accompanied by a decrease in easily hydrolyzable (amide) N, so that the total liver ammonia is unchanged. Liver amino N is increased enough to suggest that much of the increase is of hepatic origin. Depression in rate of urea synthesis from dl-alanine by liver slices from rats in hemor rhashock is increased with increasing severity of shock, relatively more than is the rate of O2 uptake. The rate of deamination of the amino acid is depressed only to about 50% of the normal rate, even in severe shock. The rate of synthesis of urea from ammonium lactate is also diminished seriously in severe shock, again relatively more so than the rate of O2 uptake. The catalysis of the reaction by ornithine takes place to a smaller degree with increasing severity of shock. In states of stress, the liver apparently may lose the capacity for carrying out reactions of energy transformation, such as are required for urea synthesis, to a greater extent than the fall in respiration rate of the tissue indicates.

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