We previously showed that endotoxin-induced lactic acidemia is initially caused by a decrease in clearance of lactic acid (L) and not by an increase in production (Pediatr Res 41:1997, 38A). Previous investigators have shown that hepatocellular function is impaired early in the course of sepsis (Wang et. al. Shock 3:1995). Because the liver is a major site of L metabolism, we hypothesized that impaired hepatic extraction of L would contribute to endotoxin-induced lactic acidemia. To test this hypothesis, we measured simultaneous hepatic venous (HV), portal venous (PV) and aortic (A) lactic acid concentrations after 2 mg/kg LPS was infused into the IVC in chronically catheterized rats (n=3). Blood L concentrations (nmol/ml) were analyzed using an enzymatic assay. The extraction of L by the liver, non-hepatic splanchnic organs, and the entire splanchnic system was determined from the hepatic venous-portal venous (HV-PV), portal venous-aortic (PV-A), and hepatic venous-aortic (HV-A) concentration gradients, respectively. Values in table are mean (SD). Aortic L concentration increased 4.5 fold peaking at 90 min post LPS infusion. The positive L(PV-A) remained unchanged indicating that the non-hepatic splanchnic organs are net producers of L but do not contribute to the increase in L after LPS. The increasingly negative L(HV-PV) after LPS indicates that the liver retains the ability to extract L from the PV after LPS. The increasingly negative L(HV-A) indicates that the splanchnic system as a whole is a net clearer of L after LPS. We conclude that the ability of the liver to extract lactate is not impaired by LPS. However, the net hepatic flux of L is related both to the concentration gradient of L across the liver and blood flow through the liver. Since L(HV-PV) becomes increasingly negative, we speculate that the decreased net extraction of lactate after LPS may be related to a decrease in hepatic blood flow.

Table 1 No caption available.
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