Am. J. Respir. Crit. Care Med.,
Volume 161, Number 2, February 2000, 517-526
Impaired Hepatic Extraction and Increased
Splanchnic Production Contribute to Lactic
Acidosis in Canine Sepsis
CARLA
CHRUSCH,
COLIN
BANDS,
DEEPAK
BOSE,
XING
LI,
HANS
JACOBS,
KRIKA
DUKE,
EDGAR
BAUTISTA,
GREGG
ESCHUN,
R.
BRUCE LIGHT,
and
STEVEN N.
MINK
Departments of Medicine, Pharmacology and Therapeutics, Anesthesiology, Physiology, and Biochemistry and Molecular Biology,
University of Manitoba, Winnipeg, Manitoba, Canada
In septic shock, the extent to which lactic acidosis (LA) is a consequence of splanchnic lactate overproduction (SLP) or impaired hepatic lactate extraction (HLE) is not clear. We examined SLP and HLE
in E. coli sepsis in dogs. We further determined the effects of vasopressor treatments, which included
phenylephrine, dopamine, norepinephrine, and a combination of dobutamine and norepinephrine treatment, on SLP and HLE in respective groups. The animals were studied while anesthetized and
ventilated. During sepsis, SLP increased 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 delivery (SOD).
During sepsis, HLE increased as compared with baseline (0.8 versus 8%, p < 0.05), but was significantly lower than that found during lactic 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 related to reduced splanchnic oxygen delivery, as well as to a decrease in hepatic lactate extraction. Effects of different vasoactive agents did
not alter either splanchnic lactate production or hepatic lactate extraction in this sepsis model.
Chrusch C, Bands C, Bose D, Li X, Jacobs H, Duke K, Bautista E, Eschun G, Light RB, Mink SN.
Impaired hepatic extraction and increased splanchnic production contribute to lactic acidosis in canine sepsis.