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 i ntact, pentobarbital-anesthetized dog model (n=14). Ultrasonic flow pr obes mere placed around the portal vein and hepatic, renal, and femora l arteries. After splenectomy, catheters were inserted into the pulmon ary artery, aorta, and hepatic, left renal, and femoral veins, Whole b lood lactate and blood gases from all catheters, organ flows, and card iac output were measured before and 30 to 45 min after a bolus infusio n of Escherichia coil endotoxin (1 mg/kg). After endotoxin infusion, m ean 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 relea se of lactate adding a mean of 9.97+/-16.23 mmol/h (p<0.05) to the sys temic 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). Exc ept for the kidney, where a decrease in blood flow correlated with dim inished uptake, there was no correlation between changes in transvisce ral lactate fluxes and organ or systemic oxygen delivery during endoto xemia, A positive correlation between lactate uptake and oxygen consum ption 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 si gnificant lactate release, and other viscera that normally take up lac tate are unable to adequately dear this increased lactate.