Hemodynamic and metabolic consequences of a 90-minute period of liver ischemia followed by 120 minutes of reperfusion were studied in rats that were awake during most of the experiment and in rats anesthetized with either pentobarbital (40 mg/kg body weight) or chloralose (30 mg/kg X hour) during the complete length of the experiment. Ischemia was induced by occluding the blood vessels to the left and median liver lobes with a small vascular clamp, which was removed after 90 minutes. Protein synthesis rate was determined by measuring incorporation rate of 14C-leucine into protein in incubated liver slices. At the end of the ischemic period, adenosine triphosphate levels in liver tissue and protein synthesis rate were reduced by 80% to 90%, with no significant differences among groups. During reperfusion, energy levels and protein synthesis rate remained depressed in the anesthetized animals, but improved, although not to normal values, in the awake rats. Hepatic tissue water increased during ischemia, probably reflecting hepatocellular membrane injury. The increase in hepatic tissue water was more pronounced in the chloralose group than in the other groups of rats. During reperfusion hepatic tissue water remained increased in the anesthetized rats but was normalized in the awake group. Mean arterial blood pressure was stable during ischemia and reperfusion in the pentobarbital anesthetized rats, while a progressive decrease in blood pressure during the experiment was noted in the chloralose group. The results suggest that hemodynamic and metabolic responses to liver ischemia and reperfusion can be influenced by anesthetics. Chloralose may be less suitable than pentobarbital for anesthesia when liver ischemia is inflicted.