Altered glucose metabolism and lactic acidemia are features of Gram-negative polymicrobial abscesses, but the relationship between carbohydrate metabolism and the aerobic or anaerobic organisms is unclear. Since reductions in the % active pyruvate dehydrogenase complex (PDHa) limits glucose oxidation in sepsis, the effect of a 7-day monoclonal (E. coli or B. fragilis) vs. biclonal (E. coli + B. fragilis) intra-abdominal abscess (IA) on PDHa and lactate concentrations in skeletal muscle (SM) and plasma was studied in rats. A chronic IA was created by the intraperitoneal introduction of a sterile rat fecal-agar pellet (1.5 ml) inoculated with a known bacterial flora [sterile (S); E. coli 106 CFU/ml (EC); B. fragilis 108 CFU/ml (BF); E. coli 103 CFU/ml + B. fragilis 104 CFU/ml (ECLBF); E. coli 103 CFU/ml + B. fragilis 108 CFU/ml (ECHBF)]. Neither SM PDHa nor SM nor plasma lactate were altered from control in animals with either sterile (S) or E. coli (EC) monoclonal IA, but SM PDHa was significantly (p < 0.001) reduced and SM lactate increased (p < 0.05) in rats with B. fragilis 108/ml (BF) monoclonal IA. In biclonal IA, the effect of sepsis on SM PDHa depended on the concentration of B. fragilis in the IA fluid (ECLBF = 104 CFU/ml vs. ECHBF = 108 CFU/ml) since the E. coli were constant (103 CFU/ml). At the lower B. fragilis IA concentration (ECLBF), the SM PDHa was not different from control. However, when the IA B. fragilis concentration was increased to 108 CFU/ml (ECHBF), the SM PDHa was significantly (p < 0.001) decreased relative to control. A decreased muscle PDHa was always associated with elevated SM and plasma lactate concentrations. These results suggest that IA which permit a threshold of relatively nonlethal (BF = 0% mortality) anaerobic B. fragilis (≥108 CFU/ml) to enter the circulation are more important in altering metabolic control of skeletal muscle glucose oxidation and in producing lactic acidemia than are IA with only aerobic E. coli. However, in biclonal intraabdominal abscesses, B. fragilis potentiated the early mortality from E. coli (EC = 6% vs. ECHBF = 37% mortality), suggesting that the metabolic effect of the B. fragilis-induced lactic acidemia is synergistic with the direct toxic effects of the E. coli.
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