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Effect of in situ hypothermic perfusion on intrahepatic pO2 and reactive oxygen species formation after partial hepatectomy under total hepatic vascular exclusion in pigs


Bob H.M. Heijnen, MD, Surgical Laboratory, IWO 1–151, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
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Abstract:Aim:  This study examined attenuation of ischemia and reperfusion (I/R) induced liver injury during liver resections by hypothermic perfusion of the liver under total hepatic vascular exclusion (THVE). Method: Reactive oxygen species (ROS) formation, microcirculatory integrity and endothelial cell damage were investigated. Left hemihepatectomy (LHX) was performed without in situ perfusion (control-LHX, n = 5) or with concomitant in situ perfusion with hypothermic (4 °C) Ringer-glucose (cold-LHX, n = 5) or normothermic (38 °C) Ringer-glucose (warm-LHX, n = 5). Glutathione (GSH) and malondialdehyde (MDA) concentrations, tissue pO2 levels and hyaluronic acid (HA) uptake capacity were determined. Results: After cold, warm and control-LHX, 24 h survival was 5/5, 0/5 and 3/5, respectively. GSH levels were best preserved after cold-LHX during reperfusion. MDA levels increased in all groups without significant differences between the groups during reperfusion. Tissue pO2 levels increased after cold-LHX whereas after warm-LHX and control-LHX, pO2 levels decreased during reperfusion. HA uptake capacity remained normal after cold-LHX. After warm-LHX and control-LHX, HA uptake capacity decreased after 6 h of reperfusion but recovered after 24 h of reperfusion in the control-LHX group. Conclusion: Moderate hypothermic perfusion protects the liver from I/R injury during LHX under THVE. This protective effect depended on maintenance of liver microcirculation rather than a reduction in ROS formation.

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