November 12, 2014
Record Number: 5329Author: Arndt, S., Meyer, F., Brandt-Nedelev, B., Wartmann, T., Lippert, H. and Halangk, W.
Title: [Implications of nutritional status for onset and characteristics of experimental acute pancreatitis in a mouse model]
Journal: Zentralbl Chir
Short Title: [Implications of nutritional status for onset and characteristics of experimental acute pancreatitis in a mouse model]
Alternate Journal: Zentralblatt fur Chirurgie
ISSN: 1438-9592 (Electronic)
Original Publication: Auswirkungen des Ernahrungszustands auf die Auspragung einer experimentellen akuten Pankreatitis der Maus.
Accession Number: 23575520
*Disease Models, Animal
Mice, Inbred Strains
Pancreatitis, Acute Necrotizing/complications/pathology/*physiopathology
Abstract: BACKGROUND: Due to uncontrolled activation of digestive enzymes produced within the pancreas, acute pancreatitis is a disease with a great potential for complications and variable course. Since the pathophysiological steps of human pancreatitis can only be inadequately investigated, various animal models were established to study the course of disease. The model of supramaximal caerulein stimulation allows to gain insights into intracellular events of the early phase of acute pancreatitis. Usually, overnight fasted animals are used for the model of acute pancreatitis to achieve a maximum zymogen granula accumulation and a standardised initial situation due to diminished secretion of CCK. Furthermore, the role of the nutritional state for pathogenesis and course of acute pancreatitis is controversially discussed. The aim of the study was to investigate the impact of the nutritional status on pancreatic injury in experimental acute pancreatitis. METHODS: Using standardised supramaximal caerulein stimulation (dose: 50 microg/kg; time intervals, 1/h; max. 7x), acute oedematous interstitial pancreatitis in fasted and non-fasted mice was induced. Pancreatic injury was locally characterised by pancreatic oedema, histopathological alterations and the release of pancreatic enzyme to the serum while systemic alterations were objectified by IL-6, CRP und pulmonal MPO. RESULTS: 1) Increased pancreatic serum enzyme levels after induction of acute pancreatitis in non-fasted animals do not reflect a greater affection of the pancreas since amylase and lipase in serum and pancreatic tissue correlate proportionally. The induction of acute pancreatitis provoked release of 1.3 % and 0.7 % of amylase and lipase, respectively, independently of nutritional status. 2) Neither local nor systemic parameters of pancreatic injury were significantly altered by the nutritional regimen. Pathohistologic investigations revealed increase of zymogen granula portion and cell size in non-fasted mice but no further differences compared with fasted animals. 3) During a 16-hour recovery period (no further caerulein injection), local and systemic parameters normalised. DISCUSSION: In the relatively mild model of pancreatitis induced by hormonal hyperstimulation, there was no greater pancreatic injury despite higher intrapancreatic enzyme accumulation in non-fasted animals indicating a steady state between potentially damaging and protective factors and mechanisms.