Acute non-traumatic pain increases the hepatic amino- to urea-N conversionin normal man

Background/Aim: Severe stress results in a catabolic state with nitrogen (N ) loss via hepatic urea synthesis, and in most situations a sensation of pa in, Our purpose was to establish whether pain per se upregulates liver func tion as to urea synthesis, Methods: Ten healthy male volunteers were investigated on 3 occasions in a crossover design, Self-controlled electrical pain was applied to the abdomi nal skin for 30 min to an intensity of 8 on a visual analogue scale from 0 to 10, Next, the electric profile was reproduced during local analgesia (me pivacaine 2.5 mg/kg bw), and the pain was scored to only 0.5, Finally, ther e was a control experiment with no intervention. Alanine infusion (1 mmol/k g/h) was started 2 h before intervention and continued throughout the inves tigation, Urea-N synthesis rate (UNSR) was estimated hourly as Urinary excr etion corrected for accumulation in body water and gut hydrolysis. Results: Pain increased the Functional Hepatic Nitrogen Clearance (FHNC) as sessed by the ratio UNSR/AAN (in the 3 h following pain) by 20% (22.7 +/- 1 .2 vs 19.0 +/- 0.7 Uh (control), p<0.05). FHNC during local analgesia was i n between (21.1+/-1.1 l/h) but not significantly different from either of t he two other experiments. Mean blood amino-N concentration (AAN) and mean U NSR were comparable in the three situations. There was no difference in ser um glucagon among experiments, but pain increased serum cortisol (452+/-15 vs 233+/-20 nmol/l (control), p<0.001) and plasma adrenaline (104+/-16 vs 5 8+/-9 pg/ml (control),p<0.05), Conclusion: Acute, severe atraumatic pain induces an increase in the abilit y of the liver to convert amino- to urea-N, and thus acts as a catabolic st imulus via regulation of liver function. The measurements of known endocrin e regulators of urea synthesis do not explain the phenomenon, The present d ata, however, suggest the hypothesis that the effects of pain were attenuat ed by local analgesia. If this is confirmed by further experiments, it woul d indicate a signal transmission to the liver which has not been previously described.