O016 ARGININE/ADMA IS A PREDICTOR FOR CARDIAC OUPUT IN SEPTIC SHOCK PATIENTS
2009
Rationale: Critical illness may impair liver mitochondrial function. We hypothesised that i.v. glutamine reverses hepatic mitochondrial dysfunction in critically-ill adults. Methods: After ethics approval, 43 critically-ill adults were randomised to receive 0.5 (n = 16), 0.3 (n = 14) or 0 g/kg/d (n = 13) i.v. alanyl-glutamine as a standalone infusion. A [1-13C]methionine breath test was performed by administering 2mg/kg [1-13C]methionine and measuring breath CO2/CO2 ratio every 15min for 3h. The test was performed at ICU admission and repeated on d5 or day of discharge from ICU, if sooner. 8 Healthy adults were tested as controls. [1-13C]methionine oxidation, reflecting hepatic mitochondrial function, was calculated as cumulative percentage dose recovered (CPDR) over 3h. Data (mean±SEM) are compared by one-way ANOVA or paired or unpaired t-tests as appropriate. Results: At ICU admission, patients had a significantly lower CPDR than controls (34.7±3.4 vs. 59.8±6.0, p = 0.005, reflecting impaired liver mitochondrial function). At d5/ICU discharge, patients who did not receive glutamine had a significantly lower CPDR compared with healthy controls (Table; p < 0.05). At d5/ICU discharge, patients receiving 0.5 g/kg/d alanyl-glutamine had a significant improvement in CPDR compared with baseline (p < 0.05), and a significantly higher CPDR than patients receiving 0 g/kd/d (Table, p < 0.05), such that their CPDR was similar to controls. Patients receiving 0.3 g/kg/d had a CPDR intermediate between the placebo group and the 0.3 g/kg/d group.
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