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Extrapancreatic organ manifestations in a moderately severe acute pancreatitis model.

Z J He, H Alho, Aimo P. T. Harmoinen, Tytti M. Ahola, ISTO H. NORDBACK

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Abstract

In order to study the extent of clinically relevant extrapancreatic organ injury in a moderately severe pancreatitis model, we examined the structural and functional features of the pancreas, lung, liver and kidney in a rat model simulating gallstone pancreatitis. The animals were divided into three groups: the low-ligation group, the high-ligation group and the control group, and sacrificed at 6, 24, 42, 60 and 96 h. In the low-ligation group, moderately severe acute pancreatitis was induced by the ligation of the common biliopancreatic duct plus intralipid intragastric injection, while controls underwent the ligation of the bile duct above the pancreas (the high-ligation group) or only sham operation (the control group) with fat injection. The pancreatitis induced hyperamylasemia, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis. Accompanied with a peak value of serum amylase activity 24 h after the induction, the kidney changes developed, characterized by decrease in urine output, increase in serum urea and creatinine, and proximal convoluted tubular damage under electron microscope. There were no pancreatitis associated lung or liver changes. These results suggest that this model can be used to study the pathogenesis and therapy of renal injury during acute moderately severe pancreatitis.

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What this paper is about

In order to study the extent of clinically relevant extrapancreatic organ injury in a moderately severe pancreatitis model, we examined the structural and functional features of the pancreas, lung, liver and kidney in a rat model simulating gallstone pancreatitis. The animals were divided into three groups: the low-ligation group, the high-ligation group and the control group, and sacrificed at 6, 24, 42, 60 and 96 h. In the low-ligation group, moderately severe acute pancreatitis was induced by the ligation of the common biliopancreatic duct plus intralipid intragastric injection, while controls underwent the ligation of the bile duct above the pancreas (the high-ligation group) or only sham operation (the control group) with fat injection. The pancreatitis induced hyperamylasemia, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis. Accompanied with a peak value of serum amylase activity 24 h after the induction, the kidney changes developed, characterized by decrease in urine output, increase in serum urea and creatinine, and proximal convoluted tubular damage under electron microscope. There were no pancreatitis associated lung or liver changes. These results suggest that this model can be used to study the pathogenesis and therapy of renal injury during acute moderately severe pancreatitis.

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Available abstract

In order to study the extent of clinically relevant extrapancreatic organ injury in a moderately severe pancreatitis model, we examined the structural and functional features of the pancreas, lung, liver and kidney in a rat model simulating gallstone pancreatitis. The animals were divided into three groups: the low-ligation group, the high-ligation group and the control group, and sacrificed at 6, 24, 42, 60 and 96 h. In the low-ligation group, moderately severe acute pancreatitis was induced by the ligation of the common biliopancreatic duct plus intralipid intragastric injection, while controls underwent the ligation of the bile duct above the pancreas (the high-ligation group) or only sham operation (the control group) with fat injection. The pancreatitis induced hyperamylasemia, pancreatic oedema, haemorrhage, acinar cell necrosis and extensive fat necrosis. Accompanied with a peak value of serum amylase activity 24 h after the induction, the kidney changes developed, characterized by decrease in urine output, increase in serum urea and creatinine, and proximal convoluted tubular damage under electron microscope. There were no pancreatitis associated lung or liver changes. These results suggest that this model can be used to study the pathogenesis and therapy of renal injury during acute moderately severe pancreatitis.

Key concepts: Medicine, Ligation, Pancreatitis, Acute pancreatitis, Pancreas, Hyperamylasemia, Kidney, Creatinine

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