Significance of hepatic mitochondrial redox potential on the concentrations of plasma amino acids following hemorrhagic shock in rats.

The changes in hepatic energy charge, hepatic mitochondrial redox potential, and plasma amino acid concentrations were examined in rats following the induction of hemorrhagic shock with mean arterial blood pressure at 50 mmHg. Hepatic energy charge and mitochondrial redox potential decreased significantly (P less than 0.001), from 0.86 +/- 0.01 to 0.49 +/- 0.05 and from 14.4 +/- 0.8 to 2.9 +/- 0.6, respectively, at 2 hours after the induction of hemorrhagic shock. Concentrations of total amino acids, alanine, proline, tyrosine, and phenylalanine in plasma increased, and molar ratio [( valine + leucine + isoleucine]/[tyrosine + phenylalanine]) in plasma decreased significantly (P less than 0.001). Hepatic mitochondrial redox potential was correlated negatively with total amino acids (r = -0.90, P less than 0.001) and positively with molar ratio (r = 0.85, P less than 0.001) during hemorrhagic shock. By reinfusion of shed blood at 2 hours after hemorrhagic shock, hepatic energy charge and mitochondrial redox potential immediately recovered to the pretreatment level. However, total amino acids, proline, tyrosine, and phenylalanine increased transiently and thereafter decreased to the pretreatment level. Molar ratio did not recover even at 60 minutes after reinfusion. These results suggest that, in hemorrhagic shock, reduced hepatic mitochondrial redox potential causes inhibition of the citric acid cycle metabolizing the amino acids in the liver and an increase of plasma amino acids; these results suggest also that, in the recovery phase from shock, the restoration of hepatic mitochondrial redox potential is a prerequisite for normalization of the accumulated plasma amino acids.