We have previously shown that gut ischemia/reperfusion (I/R) causes liver dysfunction in vivo (increased [I125]albumin leak, decreased mitochondrial redox potential). Our purpose was to investigate liver dysfunction due to gut I/R in an ex vivo model where oxygen delivery (DO2) could be controlled. Rats underwent laparotomy (sham) or 45 min of superior mesenteric artery (SMA) occlusion (I/R) and 6 hr later the gut and liver were isolated in situ. Pressures were monitored while recirculating blood was perfused via the hepatic artery (2.5 ml/min) for 90 min and the SMA (7.5 ml/min) for the first 30 min, then the portal vein (7.5 ml/min) for 60 min. Both gut and liver DO2 and VO2 (Fick method) were maintained throughout the study period in the gut I/R as well as sham groups. Despite maintenance of liver VO2, however, gut I/R resulted in a marked and persistent reduction in bile flow. In conclusion, dysfunctional bile production after gut I/R is not due to impaired VO2, but rather gut-liver signaling yet to be defined.