Abstract
In MA the major nitrogen source for ammoniagenesis is GLN and plasma levels rise within minutes after initiation of MA. GLN may be provided by increased catabolism (C) of muscle at the expense of anabolism and growth. We studied MA in an in vitro perfused muscle preparation obtained from normal, fed rats. The control perfusate consisted of Krebs-Henseleit buffer (NaCl 118 mM, NaHCO3 25 mM) with erythrocytes, glucose, albumin and amino acids. The MA buffer was identical except that 15 mM NaHCO3 was replaced by NaCl. Both perfusates were continually gassed with 95% O2/ 5% CO2. Measured pH values were 7.38 vs 6.99 at the start and 7.33 vs. 7.13 at 3 hours. Protein synthesis (S) and (C) were assessed using [14C] phenylalanine and GLN was determined spectro-photometrically. During the first hour, perfusate GIN rose higher in the MA preparations (0.303 vs. 0.188 mmol/g HC p = 0.04), but by 3h, there were no significant differences. Muscle GLN levels decreased between 1 and 3 h (-1.304 vs. -1.125 umol/g HC, p NS) so that net GLN production was no different between the the two groups. Individual S and C rates were not different but MA resulted in a 15% decrease in the rate of net muscle degradation (P 0.05). Thus, MA leads to transient redistribution of GLN between intra and extracellular spaces and to decreased and not increased muscle degradation. These results cast doubt on the importance of muscle as the source of nitrogen for ammoniagenesis in acute MA.
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Wassner, S., Li, J. 1274 MUSCLE PROTEIN TURNOVER AND GLUTAMINE (GLN) RELEASE IN ACUTE METABOLIC ACIDOSIS (MA). Pediatr Res 19, 323 (1985). https://doi.org/10.1203/00006450-198504000-01298
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DOI: https://doi.org/10.1203/00006450-198504000-01298