BACKGROUND: Surgical hepatic inflow obstructions such as the Pringle Maneuver (PM) or hepatic vascular exclusion (HVE) can reduce bleeding during hepatic resection, but ischemia/reperfusion injury of the liver and systemic hemodynamic changes are also inevitable during and after PM or HVE. Nitric oxide plays a pivotal role in ischemia/reperfusion injury. We evaluated hemodynamic changes and changes of nitric oxide during liver ischemia/reperfusion injury excluding the effects of intestinal ischemia. METHODS: Liver ischemia was induced by clamping of the portal triad, infrahepatic and suprahepatic inferior vena cava for 90 minutes. To exclude the effects of intestinal ischemia during liver ischemia, portal and iliac venous blood was bypassed to the jugular vein using a pump. Hemodynamic parameters and nitric oxide were measured serially; before and during ischemia, and after reperfusion. RESULTS: Mean arterial blood pressure (MAP) was well-maintained during ischemia, but after reperfusion, MAP, cardiac output (CO) and stroke volume (SV) significantly decreased (35 - 40, 30 - 40 and 30%, respectively) postischemia. Compared to preischemia, systemic vascular resistance and heart rate did not change after reperfusion. Pulmonary vascular resistance and mean pulmonary arterial blood pressure significantly increased (220 - 250% and 60 - 70%) after reperfusion. Nitric oxide (NO) did not change until 20 minutes after reperfusion, but after 40 minutes reperfusion, NO significantly decreased (20%) compared to preischemia. CONCLUSIONS: After 90 minutes warm liver ischemia/reperfusion causes hypotension induced by decreased CO and SV. Increased PVR seems to be the cause of decreased CO and SV. NO-SVR interaction does not seem to be the cause of postreperfusion hypotension.