Abstract

BackgroundIschemia and reperfusion injury (I/R-I) are well recognized factors contributing to acute pancreatitis after pancreas transplantation. Ischemic preconditioning (IP), i.e. short periods of ischemia followed by reperfusion prior to a sustained ischemic insult, has been reported to ameliorate I/R-I, for example in liver surgery and liver transplantation. The aim of the present study was to evaluate effects of IP on the pancreas in an animal model.MethodLandrace pigs (42 ± 3 kg) were randomly allocated to the following groups: Group A [control]: 3 hrs of warm ischemia followed by 6 hrs of reperfusion (n = 8); Group B [IP]: 5 min of ischemia followed by 20 min reperfusion prior to protocol A (n = 7); Group C [IP10/10]: 10 min ischemia, 10 min reperfusion prior to protocol A (n = 6). Animals were equipped with catheters in the carotid artery, external jugular vein and distal part of the splenic artery and vein. The celiac axis was also exposed. The pancreas was divided along the superior mesenteric vein; the head was not further mobilized and served for control measurements; complete ischemia of the tail was achieved by complete organ dissection and clamping of the splenic vessels. Blood flow through the pancreatic tail was measured before and after IP and several times following sustained ischemia. Tissue oxymetry was performed in the pancreatic head and tail by Clarke-type electrodes (LICOX, Fa. GMS, Kiel). Oxygen consumption was calculated from the pancreatic venous effluent and systemic blood gases. Immunehistochemistry was performed from biopsies taken before and after IP, and at several times after reperfusion following sustained ischemia; Granulocytes were stained with an anti-SWC-1 antibody (APAAP method), and positive cells counted in 5 high power fields (x160) per biopsy.ResultsIschemia caused significant changes in the tail of the pancreas in all parameters and groups (p < 0,01 vs. head). Ischemic preconditioning was associated with fewer adherent and migrating granulocyzes in the first hour of reperfusion (9 ± 3 vs. 18 ± 15 Gran/HPF in controls). Also, the number of granulocytes positively correlated with tissue pO2 (increased) and oxygen consumption (decreased). However, after six hours, there were no significant differences between controls and IP-groups.DiscussionObservation in the early period of reperfusion cannot exclude that IP may have a protective effect on the pancreas. However, results were not consistent and as convincing as previously reported for the liver. In the later stage IP failed to demonstrate any measurable benefit. Further studies are warranted to better define the effect of IP for the pancreas. Until then we suggest to avoid any form of pancreatic ischemia and the use of donor organs after ischemic insults for pancreas transplantation.

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