Impaired hepatic extraction and increased splanchnic production contributeto lactic acidosis in canine sepsis

In septic shock, the extent to which lactic acidosis (LA) is a consequence of splanchnic lactate overproduction (SLP) or impaired hepatic lactate extr action (HLE) is not clear. We examined SLP and HLE in E. coli sepsis in dog s. We further determined the effects of vasopressor treatments, which inclu ded phenylephrine, dopamine, norepinephrine, and a combination of dobutamin e and norepinephrine treatment, on SLP and HLE in respective groups. The an imals were studied while anesthetized and ventilated. During sepsis, SLP in creased as compared with presepsis (-0.017 versus 0.07 mmol/min, p < 0.05), but this increase could not be explained by reduced splanchnic oxygen deli very (SOD). During sepsis, HLE increased as compared with baseline (0.8 ver sus 8%, p < 0.05), but was significantly lower than that found during lacti c acid loading in nonseptic dogs. None of the vasopressor treatments had a detrimental effect on SLP. These results indicate that LA in sepsis occurs secondary to an increase in splanchnic lactate production that is not relat ed to reduced splanchnic oxygen delivery, as well as to a decrease in hepat ic lactate extraction. Effects of different vasoactive agents did not alter either splanchnic lactate production or hepatic lactate extraction in this sepsis model.