BACKGROUND/AIMS: Autodigestion and impairment of microcirculation of the pancreas play an important role in the pathogenesis of acute pancreatitis. Somatostatin with the reducing effect on the hepato-splanchnic blood flow decreases exocrine pancreatic secretion. Microcirculatory changes are central to the pathogenesis of acute pancreatitis. However, little is known about the effects of somatostatin on the pancreatic tissue oxygen pressure and acinar cell injury during acute pancreatitis. The aim was to evaluate somatostatin by measuring its effect on the pancreatic tissue oxygen pressure and acinar injury in acute pancreatitis. METHODOLOGY: Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide was measured to verify comparable disease severity. After the induction of acute necrotizing pancreatitis, animals randomly received either ringer lactate or somatostatin. Monitoring included cardiorespiratory parameters, hematocrit, amylase, pancreatic tissue oxygen pressure, and trypsinogen activation peptide levels. At the end of the experiments the 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 somatostatin did not increase pancreatic tissue oxygen pressure. There were no significant differences in plasma trypsinogen activation peptide and serum amylase levels in the animals of two treatment groups. Only somatostatin decreased pancreatic damage significantly. CONCLUSIONS: The use of somatostatin did not improve pancreatic microcirculation or trypsinogen activation peptide level in acute necrotizing pancreatitis; however, it reduced pancreatic damage. Therefore, it has a limited value in the treatment of the acute pancreatitis.
BACKGROUND/AIMS: Autodigestion and impairment of microcirculation of the pancreas play an important role in the pathogenesis of acute pancreatitis. Somatostatin with the reducing effect on the hepato-splanchnic blood flow decreases exocrine pancreatic secretion. Microcirculatory changes are central to the pathogenesis of acute pancreatitis. However, little is known about the effects of somatostatin on the pancreatic tissue oxygen pressure and acinar cell injury during acute pancreatitis. The aim was to evaluate somatostatin by measuring its effect on the pancreatic tissue oxygen pressure and acinar injury in acute pancreatitis. METHODOLOGY:Acute necrotizing pancreatitis was induced in rats by standardized intraductal bile acid infusion and cerulein hyperstimulation. Serum trypsinogen activation peptide was measured to verify comparable disease severity. After the induction of acute necrotizing pancreatitis, animals randomly received either ringer lactate or somatostatin. Monitoring included cardiorespiratory parameters, hematocrit, amylase, pancreatic tissue oxygen pressure, and trypsinogen activation peptide levels. At the end of the experiments the 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 somatostatin did not increase pancreatic tissue oxygen pressure. There were no significant differences in plasma trypsinogen activation peptide and serum amylase levels in the animals of two treatment groups. Only somatostatin decreased pancreatic damage significantly. CONCLUSIONS: The use of somatostatin did not improve pancreatic microcirculation or trypsinogen activation peptide level in acute necrotizing pancreatitis; however, it reduced pancreatic damage. Therefore, it has a limited value in the treatment of the acute pancreatitis.