Leukocyte glycolysis and lactate output in animal sepsis and ex vivo humanblood

Lactate is released in large quantity from sites of sepsis and inflammation . We asked whether the increased lactate production found in sepsis can be explained by the augmented glycolysis of inflammatory cells. The glycolytic metabolism of rat peritoneal leukocytes was measured following cecal ligat ion and perforation (CLP) or sham laparotomy. CLP augmented glucose uptake, the pentose phosphate pathway, end glucose oxidation. Lactate output incre ased from 1.03 +/- 0.05 to 1.20 +/- 0.05 fmol . cell(-1). min(-1) (P <.001) . Total lactate output of peritoneal lavage fluid increased from 7.94 +/- 2 .59 to 28.12 +/- 5.60 nmol L . min(-1) (P <.005). The effect of lipopolysac charide (LPS) on the lactate output of whole blood from 31 critically ill p atients was measured. Leukocyte lactate production was calculated by multip le linear regression analysis. Following exposure to LPS, human leukocyte l actate output increased from 0.20 +/- 0.09 to 1.22 +/- 0.14 fmol . cell(-1) . min(-1) (P <.001). This rate of production is so high that it suggests th at the lactate output of different tissue beds in sepsis may be affected by their different cell populations and state of activation. This study suppo rts the hypothesis that lactate may be more a product of inflammation than a marker of tissue hypoxia in sepsis. Copyright (C) 1999 by W.B. Saunders C ompany.