Intraoperative continuous glucose monitoring revealed that liver ischemia/reperfusion causes a rapid and profound transition in glucose concentration. We hypothesized that the washout of the glucose stored in the liver leads to a rapid transition in blood glucose concentration. Six female beagles were studied. A portosystemic shunt was established, and the glucose levels in the jugular, hepatic, and portal veins were continuously monitored. All beagles were stabilized for 30 min, and, subsequently, the hepatic artery and portal vein were clamped (the Pringle maneuver). After 30 min of warm hepatic ischemia, the clamp was removed in order to initiate hepatic reperfusion. The endpoint of the experiment was 60 min after the onset of reperfusion. The glucose levels in the abovementioned veins were recorded continuously. The glucose level in the hepatic vein increased 10 min after the start of the Pringle maneuver and was significantly higher than that in the jugular vein and portal vein just before unclamping. The glucose level in the hepatic vein peaked at 2 min after unclamping and that in the portal and jugular veins started to increase after reperfusion. The glucose level in the hepatic vein was significantly higher than that in the jugular and portal veins between 9 min after clamping and 8 min after reperfusion. In conclusion, our study among beagles showed that glucose release from the hepatic vein and sinusoid leads to a rapid elevation in systemic blood glucose levels after liver ischemia/reperfusion. This knowledge might help in the development of new strategies for blood glucose management during hepatectomy.