BIOCHEMICAL CHANGES DURING ACUTE PHYSIOLOGICAL FAILURE IN THE RAT: II. THE BEHAVIOR OF ADENINE AND PYRIDINE NUCLEOTIDES OF THE LIVER DURING SHOCK

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Abstract
The acute hypoxia, caused by severe blood loss, gives rise to the rapid breakdown of glycogen in the liver and concurrent increase in the concentration of ATP in the mitochondria. The increase in adenosine triphosphate (ATP) continues until the onset of the reversible phase of shock. The glycogen reserve approaches depletion during the late reversible phase. Simultaneously, the generation of ATP in the mitochondria ceases and the concentration begins to fall. It would appear that at this time the adenylate kinase mechanism in the mitochondrial membrane comes into play to convert the adenosine diphosphate (ADP) into ATP and adenosine monophosphate (AMP). As the condition becomes irreversible the residual ATP and phosphorylated intermediates of the Embden–Meyerhof system undergo rapid hydrolysis with liberation of AMP and inorganic phosphate in the cytoplasm.The concentration of the pyridine nucleotides undergoes no change in any of the liver cell components until the onset of the irreversible phase of failure. Thereafter, these nucleotides undergo a progressive conversion to the reduced form.

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