0.27 BRANCHED CHAIN AMINO ACID CLEARANCES IN CONTROLS AND CIRRHOTICS

G.P.Bianchi, G.A.Checchia, G.Marchesini, H.Vilstrup, D.Patrono, & M.Zoli

Istituto di Patologia Medica I, Universiti di Bologna, Division of Hepatology, Riqshos- pitalet, Copenhagen, and Laboratorio Centralizzaato, Policlinico S. Orsola, Bologna

The metabolism of the branched chain amino acids (BCAA=Valine(Val)+Iso- leucine(Ile)+Leucine(Leu)) was examined in 8 male normoqlycemic patients with cirrhosis and in 8 age and weight matched control patients. BCAA we- re given as prime-continuous infusions at a rate of 25 pmol/(min*kq BW), increasing the concentration of BCAA to a steady state of 5600 pmol/l in the interval 120 to 150 min. The plasma clearances of Val, Ile, and Leu, calculated for each BCAA as infusion rate divided by steady state concen- tration, were 4.4 + 0.8 ml/set (mean+SD), 6.0 + 1.3 ml/set, and 5.6 + 1.0 ml/set, respectiveiy. The clearances-were not different between controls and cirrhotics but different among the different BCAA (~(0.01, l-way ana. of var.). After infusion stop the concentration of each BCAA decreased li- nearly in semi-log plots indicating first order kinetics, supporting the use of the clearance concept. The theoretical volumes of distribution for Val, Ile, and Leu, calculated as clearance divided by elimination con- stant, were 72 + 15% of body weight in controls (not different among BCAA), and 74 +-19%, 48 + 15%, and 59 + 15%, respectively, in cirrhotics, the two last volumes being lower than Tn controls (~(0.025, t-test), pre- sumably reflecting decreased mucsle mass in cirrhotics. The decreased concentration of BCAA in cirrhotics (in the present patients from 500 to 400 pmol/l) is not attributable to changes in the elimination of the BCAA from plasma. The most likely explanation is decreased input of BCAA to plasma, viz. decreased protein intake or break down.

0.28 THE EFFECT OF TWO INTRAVENOUS NUTRITIONAL REGIMENS UPON THE MUSCLE FREE INTRACELLULAR (ic) AMINO ACID (AA) POOL IN SEVERE INJURY K. Sicking, R. Abele, 3. Zander, M. Benedik- ter, I. Hirschmiiller-Ohmes, P. Fiirst, Ch. Puchstein (Dept. of Anaesth. and Intensive Care , Univ. Mijnster and Inst. Biol. Chem. and Nutr., Univ. Hohenheim, FRG)

The aim of the present study was to evaluate whether aggressive nutritional efforts with variation in the energy source may beneficially influence ic muscle free AA pattern in severely ill patients. 25 patients after accidental injury were randomized in two groups to receive isoenergetic (35 kcal/kg BW) and isonitrogenous (0.24 g N/kg BW) TPN during 6 days. 12 patients received 6.0 g glucose and 0.5 g fat (G-group) and 13 patients were given 3.5 g glucose and 1.7 g fat (F-group) per kg BW. Free AA were determined on the lst, 3rd and 6th day after injury in muscle (needle biopsy) and plasma samples. On the first postinjury day plasma free AA decreased but Glu, whereas 3 and 6 days after the trauma normal or elevated levels were observed; the increase was more pronounced in the G-group than in the F-group. Muscle free Gln level was reduced with 40% and 70% immedia- tely after the trauma in the G-group and in the F-group, respectively. Muscle free BCAA, Phe and Ala concentrations considerably increased 1 day after the injury; again the ele- vations were more profound in the G-group than in the F-group. A successive decline of muscle free Gln in the G-group and a further elevation of BCAA and Phe were observed on the 3rd postinjury day. The concentrations of basic AA (Lys, Arg, Orn) were uniformly declined in both groups, remaining low throughout the study. The initial differences in muscle free AA between the groups disappeared 6 days after injury. It is to conclude that ic transport and/or cellular energy charge might be influenced by the high supply of glucose in the immediate postinjury phase, thereby effecting ic AA concentrations. The results may thus emphasize the role of glucose in maintaining cellu- lar glycogen and presumably facilitating cellular ATP resynthesis. The fact that the same pathological ic pattern was apparent 6 days after injury may however suggest that prolonged surgical hypermetabolism might be associated with seriously deranged cellular energy metabolism (sick cell syndrome?) little influenced by aggressive nutritional efforts irrespective of amount and kind of energy substrate given.

44