Muscle and plasma amino acids following injury. Influence of intercurrent infection.

Abstract

The present study was undertaken to determine intracellular amino acid patterns in patients with multiple trauma, whether or not complicated by sepsis and during convalescence. A percutaneous muscle biopsy was performed three to four days following major accidental injury in ten patients and analyzed for muscle free amino acids. Venous blood was drawn at the time of the biopsy and analyzed for plasma free amino acids. Five patients developed sepsis and a repeat biopsy was performed on days 8 to 11. In five of the patients a biopsy was performed during the late convalescent period (anabolic phase). A marked depletion of nonessential amino acids in muscle occurred in both injury and sepsis due to a decrease (50%) in glutamine, which was equally marked in both states. The essential amino acids in muscle increased in injury. During sepsis, a further increase was observed with a return toward normal in the convalescent period. In injury, the most marked rise was in the branched-chain amino acids, phenylalanine, tryosine and methionine. With sepsis, a further rise in muscle branched-chain amino acids, phenylalanine and tryosine occurred, while plasma levels remain unchanged. During convalescence, muscle glutamine, arginine, histidine and plasma branched-chain amino acids were below normal, whereas muscle phenylalanine and methionine were elevated. The muscle free amino acid pattern observed after major trauma was essentially the same as earlier described following elective operation. This suggests a common response of intracellular amino acids irrespective of the degree of injury, and may indicate that the pump settings which regulate amino acid transport follow the "all or none" rule. The high intracellular levels of branched-chain amino acids in sepsis suggest that the energy deficit of this state is due to an impairment of substrate use rather than intracellular availability. The high concentrations of the aromatic amino acids and methionine may be due to altered liver function. During the late convalescent period (anabolic phase) the low levels of certain key amino acids suggests inadequate nutrition. The difficulties in nourishing the injured or septic patient are well recognized. The period following these catabolic states may be an important period for the application of an optimal, aggressive nutritional regimen.