The effects of prostaglandin E1 on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats

BACKGROUND/AIMS: In this study we investigated the effects of prostaglandin E1 on the microperfusion of the pancreas during acute necrotizing pancreatitis in rats. METHODOLOGY: Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptides were measured to verify comparable disease severity. After the induction of acute pancreatitis, animals randomly received either ringer lactate or prostaglandin E1. Monitoring included cardiorespiratory parameters, hematocrit, pancreatic oxygen tissue oxygen pressure, serum amylase and trypsinogen activation peptides. At the end of experiments pancreas was removed for evaluation of acinar cell injury. RESULTS: The two study groups were comparable with regard to mean arterial pressure, heart rate, arterial blood gases, hematocrit, and serum amylase. The induction of pancreatitis resulted in the significant decrease of pancreatic tissue oxygen pressure. In both groups the use of prostaglandin E1 did not change pancreatic tissue oxygen pressure despite of stable cardiorespiratory parameters, and serum amylase activity. Prostaglandin E1 decreased pancreatic damage and serum trypsinogen activation peptide level significantly. CONCLUSIONS: These results suggest that prostaglandin E1 had no effects on the improvement of microcirculation of pancreas, and had beneficial effects on the course of acute necrotizing pancreatitis.