Temporary pancreatic duct occlusion by ethibloc: cause of microcirculatory shutdown, acute inflammation, and pancreas necrosis.

Abstract

Temporary obliteration of the pancreatic duct has been suggested to be beneficial in chronic pancreatitis, segmental pancreatic transplantation, and following Roux-Y pancreaticojejunostomy. Little is known, however, as to whether obliteration of the duct alters exocrine pancreatic physiology. Therefore we studied in male inbred Lewis rats the immediate effects of Ethibloc-induced duct obliteration (Ethibloc: Ethicon, Norderstedt, Germany) on pancreatic microcirculation, inflammation, and tissue injury (n = 8), and compared these effects with those caused by experimental pancreatitis (4% sodium taurocholate; n = 8). Animals receiving an intraductal infusion of saline served as controls (n = 8). Duct occlusion with Ethibloc resulted in a marked decrease (p < 0.05) in capillary red blood cell (RBC) velocity and functional capillary density (FCD) to 88 +/- 39 microm/s (baseline 716 +/- 40 microm/s) and 72 +/- 33 cm(-1) (baseline 493 +/- 21 cm(-1)), respectively, which was even more pronounced when compared with that observed in experimental pancreatitis (333 +/- 62 microm/s and 195 +/- 44 cm(-1), respectively). In parallel, the manifestation of tissue damage was found to be more severe after Ethibloc; and chloracetate esterase staining showed a larger number of infiltrating leukocytes [555 +/- 86/high power field (HPF) versus pancreatitis: 160 +/- 12/HPF; p < 0.05). We conclude that intraductal application of Ethibloc induces significant microcirculatory failure and a marked inflammatory response, which are even more pronounced when compared with the changes observed with experimental pancreatitis. Based on these results and the fact that there is no direct proof for a benefit of temporary duct occlusion by Ethibloc, it is proposed that the procedure be reevaluated for its use in pancreatic surgery.