P71 INFLUENCE OF TPN ON MUSCLE AMINO ACID OUTPUT IN SEPTIC PATIENTS X. Leverve, F. Carpentier, J. P. Caravel, M. Guignier. CHU de Grenohle, 38043 Grenoble Cedex, France

Muscle catabolism was studied in patients with severe peritonitis by daily assays of urinary 3 Methylhistidine (3 MeHis), nitrogen, and fe- moral arterio-venous differences of a.a., w'thout TPN, then 48 rs an 8 days after -1 0 30 g of N x Kg -Q x d-f

and leg blood output (133 X5],, d tarting TPN : 55 KCal x Kg

(Azonutril (R 5 ). After 48 hrs of TPN we ob- servid a dramatic reduction in muscle catabolism: 3 MeHis down 44 % with respect to the initial value (p<O.OOl) decrease of leg a.a. output : 604 + 103 to 254 + 87 nM x mn-1 x 100 g (iii t sem) (p<O.O05), decrease essentially 07 essential a.a. (-57 %) i-e. aromatic a.a. (-69 %) and branched chain a.a. (-91 %). Comparing the results of 48 hrs and 8 d, we observed no decrease in 3 MeHis, however leg a.a. output was close to zero (-68 + 46), with a reduction notably in the essential a.a. (-89%). There exists a strorgrelationship between 3 MeHis and nitrogen balance for the entire study group (3 MeHis = -15.3 x N balance t 278 : r = 0.8019 : = 3 90) as well as for each subject individually (r = 0.8062 t 0.073 : n = 10). These results suggest that in long term septic hyper&abolic states the use of TPN first reduces muscle catabolism (decrease of 3 MeHis and leg a.a. output) and secondly increases muscle protein synthesis without modifying b-eakdown (3 MeHis stable, and continued reduction in leg a.a. output).

P72 DO AMINO ACID SOLUTIONS INDUCE METABOLIC ACIDOSIS IN SEVERE SEPTIC PATI- ENTS ? J-F.Dhainaut, V.Fourestie, J.F.Monsallier, J.Bons, B.Schlemner and A.Carli. Intens.Care Unit. Univ.Hop.Cochin, Paris, France.

Amino acid (AA) solutions induced-hyperchloremic acidosis in severe sep- tic patients (pts) during total parenteral nutrition (TPN) was suspected but not investigated. To evaluate the changes in acid base status, 20 such adult pts (49 yrs) were studied, no pts had other cause of acid production or bicarbonate loss. They received TPN with 40 Cal/kg/day of glucides (without lipids), 0.23 g/kg/day of nitrogen using AA solution containing 15.3 g/l of cationic AA and 5.3 g/l of basic anionic AA. We measured am- moniuria (NH4 u), titratable acidity (TA), urinary net acid excretion (NAE), nitrogen balance (NB) and arterial blood gases during the first 4 days of an hypercatabolic septic period (HSP) and during the first 4 dasy of the stable period (SP) after successful1 treatment of the septic episod.Results: pH, standard bicarbonate and Pa CO2 did not change.

Dl D2 D3 D4 D'l D'2 @ D'3 D'4 NH mEi/:

70214 90222 87220 83+24 73+14 67+15* 60+17* 56+10*

ta mEq/d

38+12 61239 50522 54+27 50+25 49+15 41% 3 35+ 9

NAE mEq,d IO8+I9 151250 137238 137+51 123+31 116+24 101+21 90+18*

NB * * * f

g/d -8.422.8 -7k2.8 -6.4t3.4 -4.3+3* -1.4~2.9t0.l~1.9+1.7+1.5+2.7+1.4

*pC 0.05 vs D2 (TPN was initiated from DI) Conclusion: In severe septic patients H+ production during TPN is elevated (essentially during HSP) but does not exceeds renal excretion capacity.

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