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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By.CAuSE OF conflicting reports in the literature cor~cernmg~ the effects of plaStic containers on/red blood cells (1-7), r has been and still is some hesitatio~ in substituting plastic for glass containers for blood storage. As evidence of tl~ uncertainty, there is the known fact that many! of the blodd banks ,are still using both types of container indiscriminately., xni order to throw ligh[ upon the problem, our present investigation was ~'~tertaken with the practical objective of finding out which is less deti'imental to/red! blood coils. Howev.er, it must be

Shock was produced in the albino rat by means of a standardized method of blood removal. Coenzyme A (CoA) was extracted from the liver and estimated during the reversible and the irreversible phases of shock. The assay procedure was designed so that each animal served as its own "control".The CoA concentration in the liver fell rapidly during the first half hour of shock and thereafter at a progressively slower rate as the state of shock became more severe. Escape of the coenzyme from the mitochondria and the nucleus into the cytoplasm of the liver cells became evident during the reversible phase, and its breakdown in the cytoplasm began with the onset of the irreversible phase. Even at death, however, the CoA concentration of the liver was rarely lower than 35% of the original concentration. It is unlikely, therefore, that the decrease in the CoA content of the liver is a key factor in the initiation of the state of irreversibility in hemorrhagic shock.