Effect of Injury, Sepsis, and Parenteral Nutrition on High‐Energy Phosphates in Human Liver and Muscle

This study examined the effect of varying degrees of resting hypermetabolism and total parenteral nutrition on muscle and hepatic high‐energy phosphates. Twelve severely injured patients, five critically ill patients with normal blood pressure, and six severely ill patients on 1 wk of total parenteral nutrition were investigated, and the results were compared with those in 14 normal controls. High‐energy phosphates were not significantly changed in liver and muscle after severe injury; lactate and pyruvate levels in both tissues were increased; glycogen levels in the liver were decreased. In critical illness, muscle and hepatic adenosine triphosphate as well as adenosine diphosphate were decreased significantly; energy charge potential dropped; adenosine monophosphate, lactate, and the ratio of lactate to pyruvate were increased. Liver glycogen, but not muscle glycogen, dropped remarkably. The correlation coefficient between hepatic and muscle adenosine triphosphate was 0.61. In patients on 1 wk of total parenteral nutrition, hepatic and muscle high‐energy phosphates were not significantly changed before or during total parenteral nutrition. Alterations in the adenosine triphosphate‐adenosine diphosphate‐adenosine monophosphate system in liver and muscle suggest a low‐energy charge in severe injury and critical illness. This would indicate a decreased capacity for biosynthetic reactions and production of storage compounds. The changes of high‐energy phosphates in liver are always parallel to changes in muscle. (Journal of Parenteral and Enteral Nutrition 9 :28–33, 1985)