Abstract
The aim of the present study was to investigate the pancreatic exocrine function in a canine model and to analyze the changes in organelles of pancreatic acinar cells during the early stage of acute pancreatitis (AP). AP was induced by retrograde injection of 5% sodium taurocholate (0.5 ml/kg) into the main pancreatic duct of dogs. The induction of AP resulted in serum hyperamylasemia and a marked reduction of amylase activity in the pancreatic fluid (PF). The pancreatic exocrine function was markedly decreased in subjects with AP compared with the control group. After the induction of AP, histological examination showed acinar cell edema, cytoplasmic vacuolization, fibroblasts infiltration, and inflammatory cell infiltration in the interstitium. Electron micrographs after the induction of AP revealed that most of the rough endoplasmic reticulum (RER) were dilated and that some of the ribosomes were no longer located on the RER. The mitochondria were swollen, with shortened and broken cristae. The present study demonstrated, in a canine model, a reduced volume of PF secretion with decreased enzyme secretion during the early stage of AP. Injury of mitochondria and dilatation and degranulation of RER may be responsible for the reduced exocrine function in AP. Furthermore, the present model and results may be useful for researching novel therapeutic measures in AP.
Highlights
Acute pancreatitis (AP) is a common, often life-threatening, inflammatory disease of the exocrine pancreas and is associated with a significant morbidity and mortality [1,2]
The protein concentration in the pancreatic fluid (PF), shown in Fig D in S1 Data, markedly decreased after the induction of AP and gradually increased but was significantly lower than that in the control group. These results indicated that the basal PF secretion and enzyme secretion were reduced during the early stage of AP (Fig 1)
Fig A and Fig B in S2 Fig show the appearance of normal pancreatic acinar cells, which were pear-shaped with round nuclei located in the base, and each nucleus had 1 or 2 nucleoli
Summary
Acute pancreatitis (AP) is a common, often life-threatening, inflammatory disease of the exocrine pancreas and is associated with a significant morbidity and mortality [1,2]. Multiple factors are involved in the initiation and development. Reduced Pancreatic Exocrine Function in AP of AP, making it difficult to choose specific or effective treatments for the prevention of complications. A common feature in AP is the intra-acinar cell activation of zymogens, leading to autodigestion of the gland [3,4]. The focus of research has been on signaling pathways involved in the inflammatory cell infiltrate and the systemic inflammatory response [4,5,6,7,8,9]
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