Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2025
A porcine model of acute necrotizing pancreatitis.
СтатьяНазвание и аннотация: Перевод в очереди
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Steiner Joerg M, Algül Hana, Ruess Dietrich A, Demir Ihsan Ekin, Braren Rickmer, Schwamberger Sabine, Lesina Marina, Reiser Judith, Werner Julia, Groll Tanja, Metzler Thomas, Steiger Katja
Аннотация
BACKGROUND/OBJECTIVES: Acute necrotizing pancreatitis is a common disease in humans and leads to significant and world-wide morbidity and mortality. Exploration of new pharmaceutical agents for the treatment of this disease frequently rests on rodent models that may not be relevant for spontaneous human disease and also preclude collecting multiple blood samples. Goal of this project was to establish an experimental model for acute necrotizing pancreatitis in pigs that mirrors the development of systemic complications of acute pancreatitis in humans as a prelude to clinical trials in humans.
METHODS: The accessory pancreatic duct was surgically isolated in domestic pigs and 8 μmol/kg glycodeoxycholic acid were slowly injected into the duct, followed by ligation and cutting the duct. Pigs were repeatedly evaluated clinically and multiple blood samples were collected before the pigs were sacrificed and their organs histopathologically assessed after 1, 5, or 7 days.
RESULTS: All pigs showed clinical and clinical pathological evidence of pancreatitis after induction of pancreatitis. Pigs showed histopathological evidence of acute necrotizing pancreatitis one day after induction of pancreatitis. At 7 days after induction of pancreatitis, dramatic regeneration could be observed in the pancreas. At 5 days after induction of pancreatitis, evidence of necrotizing pancreatitis was present with less evidence of regeneration.
CONCLUSIONS: The porcine model for acute necrotizing pancreatitis described here shows many parallels to spontaneous human disease and its systemic complications and may thus serve as a good model to assess the efficacy of novel pharmaceutical agents for the treatment of acute pancreatitis in humans.
METHODS: The accessory pancreatic duct was surgically isolated in domestic pigs and 8 μmol/kg glycodeoxycholic acid were slowly injected into the duct, followed by ligation and cutting the duct. Pigs were repeatedly evaluated clinically and multiple blood samples were collected before the pigs were sacrificed and their organs histopathologically assessed after 1, 5, or 7 days.
RESULTS: All pigs showed clinical and clinical pathological evidence of pancreatitis after induction of pancreatitis. Pigs showed histopathological evidence of acute necrotizing pancreatitis one day after induction of pancreatitis. At 7 days after induction of pancreatitis, dramatic regeneration could be observed in the pancreas. At 5 days after induction of pancreatitis, evidence of necrotizing pancreatitis was present with less evidence of regeneration.
CONCLUSIONS: The porcine model for acute necrotizing pancreatitis described here shows many parallels to spontaneous human disease and its systemic complications and may thus serve as a good model to assess the efficacy of novel pharmaceutical agents for the treatment of acute pancreatitis in humans.