| Abstrakt: |
Specific metal deficiencies have been reported to affect patients receiving total parenteral nutrition (TPN). Our previous studies on the topic were devoted to the computer-based interpretation of the extra urinary excretion of zinc; a theoretical approach was also proposed, with a view to compensating for the extra losses of this metal. Similarly, the present work deals with the problem of TPN-induced copper deficiency and its remedy. As is the case for zinc, the TPN-induced excretion of copper clearly stems from the relative mobilization of the plasma protein-bound pool of this metal into its diffusable low-molecular-weight fraction; this phenomenon being due to the competitive complexation of copper by the amino acids of the nutritive solution. The computer simulation of this effect thus required that first the equilibrium constants be experimentally determined for the main complexes of copper that might form in the solution as well as in plasma during the infusion. Accordingly, complex formation in the copper-histidine ternary systems with threonine, lysine, glycine, phenylalanine, valine, and cystine was investigated by potentiometry at 37 degrees C in NaCIO4 0.15 mol X dm-3. The implications of the results obtained are discussed with regard to the interpretation of the copper excretion and the estimation of the desirable daily dose of this metal for the TPN mixture under consideration. |
