Abstract
Introduction. Pancreatic injury can manifest after major hepatectomy under vascular control. The main mechanism involved seems to be remote oxidative injury due to “spillage” of reactive oxygen species and cytokines from the liver. The aim of this study is to evaluate the role of desferrioxamine in the prevention of pancreatic injury following major hepatectomy. Methods. Twelve Landrace pigs were subjected to a combination of major hepatectomy (70–75%), using the Pringle maneuver for 150 minutes, after constructing a porta-caval side-to-side anastomosis. The duration of reperfusion was 24 hours. Animals were randomly divided into a control group (n = 6) and a desferrioxamine group (DFX, n = 6). DFX animals were treated with continuous IV infusion of desferrioxamine 100 mg/kg. Pancreatic tissue injury, c-peptide and amylase concentrations, and pancreatic tissue oxidative markers were evaluated. Results. Desferrioxamine-treated animals showed decreased c-peptide levels, decreased acinar cell necrosis, and decreased tissue malondialdehyde levels 24 hours after reperfusion compared with the control group. There was no difference in portal pressure or serum amylase levels between the groups. Conclusions. Desferrioxamine seems to attenuate pancreatic injury after major hepatectomy under vascular control possibly by preventing and reversing production and circulation of oxidative products.
Highlights
Pancreatic injury can manifest after major hepatectomy under vascular control
Ischemia and reperfusion injury that occurs during liver transplantation, liver resections under vascular control, and liver trauma surgery has an impact on the liver as well as remote organs [6, 8, 11, 13, 17, 18]
Desferrioxamine has been commonly used in ischemia and reperfusion injury [23,24,25] and has been shown to attenuate ischemic and oxidative injuries to the liver and other tissues [12, 26,27,28,29,30,31,32,33], as well as remote injury to the intestinal mucosa, the lung, and the myocardium [11, 13, 17]
Summary
Pancreatic injury can manifest after major hepatectomy under vascular control. The main mechanism involved seems to be remote oxidative injury due to “spillage” of reactive oxygen species and cytokines from the liver. Desferrioxamine seems to attenuate pancreatic injury after major hepatectomy under vascular control possibly by preventing and reversing production and circulation of oxidative products. Ischemia and reperfusion injury takes place during major hepatectomies due to the need for the use of vascular control techniques, as well as in liver transplantation and liver trauma. Such maneuvers are invaluable in preventing excessive blood loss, they result in the production of cytokines and reactive oxygen species (ROS), which are responsible for induction of oxidative stress to the liver as well as to distant organs [1, 2]. Most often pancreatic injury can be subclinical, it can manifest as severe pancreatitis resulting in multiple organ failure, increasing morbidity and mortality following liver surgery [9, 10]
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