Survival and morphology of isolated pancreatic acinar cells from rats with induced acute pancreatitis are not improved with anti-inflammatory drugs.
The influence from anti-inflammatory drugs on cellular damage of pancreatic acinar cells after induction of an acute pancreatitis (AP) in a rat model was investigated. Necrotizing pancreatitis was induced by retrograde instillation of trypsin solution in the pancreatic duct (group I). The severity of inflammation was determined using morphological and histological parameters 6, 24, and 48 h after induction of the necrotizing pancreatitis. After isolation of acinar cells, the degree of damage was measured by trypan blue exclusion--a parameter of membrane permeability--as well as accumulation of rhodamine 6G--a parameter of the mitochondrial membrane potential. In groups II-V, rats were treated with the anti-inflammatory drugs indomethacine, hydrocortisone, cimetidine, and acetylsalicylic acid (ASS) before induction of AP. There was no significant benefit from therapy in either group regarding cell membrane damage, cellular energy metabolism, or histology.
Department of Surgery, UMD-New Jersey Medical School, Newark 07103, USA.
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Richter
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Matthias
D000208:Acute Disease; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002469:Cell Separation; D002470:Cell Survival; D002478:Cells, Cultured; D005260:Female; D008564:Membrane Potentials; D010179:Pancreas / Q000187:drug effects* / Q000473:pathology; D010195:Pancreatitis / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar
D000893:Anti-Inflammatory Agents