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Transvisceral Lactate Fluxes During Early Endotoxemia

      The pathogenesis of hyperlacticemia during sepsis is poorly understood. We investigated the role of lung, kidney, gut, liver, and muscle in endogenous lactate uptake and release during early endotoxemia in an intact, pentobarbital-anesthetized dog model (n= 14). Ultrasonic flow probes were placed around the portal vein and hepatic, renal, and femoral arteries. After splenectomy, catheters were inserted into the pulmonary artery, aorta, and hepatic, left renal, and femoral veins. Whole blood lactate and blood gases from all catheters, organ flows, and cardiac output were measured before and 30 to 45 min after a bolus infusion of Escherichia coli endotoxin (1 mg/kg). After endotoxin infusion, mean arterial blood lactate level increased from 0.92±0.11 to 1.60 ±0.15 mmol/L (p<0.0001). Lung lactate flux changed from uptake to release of lactate adding a mean of 9.97 ± 16.23 mmol/h (p<0.05) to the systemic circulation. Liver and muscle lactate fluxes remained neutral at all times, while kidney and gut took up lactate from the circulation both before and after endotoxin infusion (mean renal uptake, 2.73±3.85 mmol/L; p<0.001; mean gut uptake, 2.46±2.31 mmol/h; p<0.002). Except for the kidney, where a decrease in blood flow correlated with diminished uptake, there was no correlation between changes in transvisceral lactate fluxes and organ or systemic oxygen deliveiy during endotoxemia. A positive correlation between lactate uptake and oxygen consumption during endotoxemia was seen for both gut (p<0.0001) and kidney (p<0.002). We conclude that, in the dog, the pathogenesis of endotoxin-induced hyperlacticemia is complex. The lung may be responsible for significant lactate release, and other viscera that normally take up lactate are unable to adequately clear this increased lactate.

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