0101. Early and severe impairment of lactate clearance in endotoxic shock is not related to liver hypoperfusion: preliminary report

This study is part of a major project exploring the influence of adrenergic stimulation and blockade over the determinants of lactate production and utilization in septic shock. Eight anesthetized sheep subjected to a multimodal hemodynamic/perfusion assessment including pulmonary artery, hepatic and portal vein catheterizations, portal/hepatic artery flow, gut tonometry, sublingual microcirculation, muscle microdialysis and hepatic mitochondrial high-resolution respirometry, were randomized to LPS or sham. LPS sheep received 5 mcg/kg bolus (E coli O127:B8®) and then 4 mcg •kg-1•hr-1 for the rest of the experiment [2]. After 1h they were volume resuscitated. Sampling and exogenous lactate clearances were performed at 4 points (fig 1)

LPS sheep presented an early hyperlactatemic hyperdynamic septic shock and an increased muscle lactate production compared to sham (MAP 63 vs 87 mmHg; MPAP 20 vs 10 mmHg; CO 3.7 vs 2.5 l/min; arterial lactate 6.1 vs 2.6 mmol/l). Total liver flow (865 vs 692 ml/min), proportion of liver flow/CO, O₂ liver extraction, liver enzymes, and mitochondrial function were comparable between LPS and placebo (fig 2)

However, LPS sheep presented an early severe and persistent decrease in lactate clearance (C: 575 vs 1188 and D: 907 vs 1410 ml/kg/h), fig 3