ABSTRACT
BACKGROUND: The pringle maneuver (PM), hepatic inflow occlusion, during hepatic surgery reduces intraoperative bleeding and blood transfusion requirement, but hepatic ischemia/reperfusion injury is inevitable. During ischemia, xanthine oxidoreductase is converted to xanthine oxidase (XO), which can serve as a critical source of reactive oxygen species (reduces O2 to O2 .-) that contribute to inflammatory signaling, ischemia-reperfusion injury, and an impaired vascular function. The purpose of the present study was to follow changes of XO activity and O2 .- production during hepatic surgery under PM. METHODS: Eleven patients that underwent hepatectomy under intermittent PM were studied. Blood was withdrawn before PM, and 10 and 20 minutes after final reperfusion. Plasma XO activity was measured using a spectrophotometer after incubating plasma with/without xanthine for one-hour. Superoxide (O2 -) production was followed by measuring by cytochrome c reduction by plasma XO. RESULTS: After final reperfusion, plasma XO activity had increased four-fold (0.36 +/- 0.06 to 1.25 +/- 0.25 mU/ml) with a concomitant increase in O2 .- production (0.66 +/- 0.29 to 1.66 +/- 0.40microM/min). CONCLUSIONS: Significantly more XO is released into the systemic circulation after intermittent PM, with subsequently increased O2 .- production. The significant contribution of XO to hepatic surgery under PM might be beneficially managed using an anesthetic with a known antioxidative effect.