• Helge Kleinhans, Oliver Mann, Paulus G Schurr, Jussuf T Kaifi, Bente Hansen, Jakob R Izbicki, and Tim Strate.
• Department of General-, Visceral- and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany.
• World J Gastroentero. 2006 May 14;12(18):2914-8.

AimMicrocirculatory dysfunction and free oxygen radicals are important factors in the pathogenesis of severe acute pancreatitis. Additional oxygen delivery might enhance lipid peroxidation but may also improve pancreatic microcirculation. This study assesses the effect of free cellular bovine hemoglobin on the formation of oxygen radicals and microcirculation in a rodent model of severe acute pancreatitis.MethodsFifteen minutes after induction of acute pancreatitis Wistar rats received either 0.8 mL bovine hemoglobin (HBOC-200), hydroxyethyl starch (HES) or 2.4 mL of normal saline to ensure normovolemic substitution. After 6 h of examination the pancreas was excised and rapidly processed for indirect measurement of lipid peroxidation products malondialdehyde (MDA) and reduced glutathione (GSH) in pancreatic tissue.ResultsThe single application of HBOC-200 improved pancreatic microcirculation and reduced histopathological tissue damage significantly. Tissue concentration of MDA did not differ between the groups. Also no differences in GSH levels were detected.ConclusionThough the single application of HBOC-200 and HES improve pancreatic microcirculation, no differences in lipid peroxidation products were detected. The beneficial effect of additional oxygen supply (HBOC-200) does not lead to enhanced lipid peroxidation.

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