The influence of hepatic venous oxygen saturation on the liver's syntheticresponse to metabolic stress

Hepatic oxygen consumption (HVO2) and hepatic venous oxygen saturation (Shv O2) were assessed in the isolated perfused rat liver under conditions that mimic critical illness in an effort to assess their utility in predicting t he functional status of the liver. Flow rates were adjusted over the physio logic range of oxygen transport as indicated by the hepatic venous O-2 satu ration range of 10%-75%. HVO2, was found to be transport (HDO2) dependent o nly when perfusate conditions contained an increased counterregulatory horm one (glucagon, epinephrine, dexamethasone) stimulus or a high lactate conce ntration. In the absence of a metabolic load, (substrate and hormone-free p erfusate), HVO2 was transport independent even at an ShvO2 as low as 10%, A lthough transport dependency of HVO2 is frequently used to infer tissue isc hemia, hepatic oxygen consumption was poorly correlated with synthetic func tion under all conditions. In contrast, hepatic albumin production was dire ctly related to ShvO2 at all levels of HDO2 and under all perfusion conditi ons indicating that this metabolic process is particularly sensitive to red uctions in oxygen availability, which is more reliably predicted by venous saturation measurements. However, glucose and urea synthesis were almost in dependent of ShvO2. These findings indicate that various hepatic processes are affected differentially by stress conditions and flow alterations that may exist during critical illness, and protein synthesis is particularly se nsitive to oxygen deprivation. Additionally, hepatic venous oxygen saturati on measurement, but not HVO2 serves as a useful surrogate marker for hepati c albumin production suggesting that regional venous oximetry may play an i mportant role in the detection of hepatic functional impairment.