Asynchronous impairment of calcium homoeostasis in different acinar cells after pancreatic duct obstruction in rat

2002 ◽  
Vol 102 (6) ◽  
pp. 615 ◽  
Author(s):  
Aránzazu URUÑUELA ◽  
Manuel A. MANSO ◽  
Ana Ma DE LA MANO ◽  
Sara SEVILLANO ◽  
Alberto ORFAO ◽  
...  
2002 ◽  
Vol 102 (6) ◽  
pp. 615-622 ◽  
Author(s):  
Aránzazu URUÑUELA ◽  
Manuel A. MANSO ◽  
Ana Ma DE LA MANO ◽  
Sara SEVILLANO ◽  
Alberto ORFAO ◽  
...  

Current evidence suggests that alterations within acinar cells are responsible for the development of acute pancreatitis. After inducing acute pancreatitis in rats by pancreatic duct obstruction, we analysed, using flow cytometry, the progressive changes in cytosolic Ca2+ concentrations in individual acinar cells from the earliest stages to 48h after obstruction to investigate whether parallel alterations in the homoeostasis of Ca2+ could be defined in the different acinar cells throughout the evolution of pancreatitis. Morphological alterations of the pancreas, related to the severity of the disease at different stages, were observed by electron microscopy. Hyperamylasaemia and progressively more severe alterations, such as vacuolization, dilatation of endoplasmic reticulum, accumulation of zymogen granules and reorientation towards basolateral membrane, were observed during the first 12h after pancreatic obstruction. A significant increase in cytosolic Ca2+ concentration was measured at these stages in a particular type of acinar cells (R1) differentiated by flow cytometry with low forward scatter (FSC), whereas another representative group of cells (R2) with higher FSC values were able to maintain resting cytosolic Ca2+ concentrations up to 24h after obstruction. Longer periods of pancreatic duct obstruction induced disturbances in Ca2+ homoeostasis in all acinar cells. A similar increase in cytosolic Ca2+ load was reached in both R1 and R2 cells when acute pancreatitis was completely developed. In conclusion, the homoeostasis of Ca2+ in acinar cells is asynchronously impaired during the development of acute pancreatitis; cells with higher FSC (R2) appear to be more resistant than R1 cells.


2003 ◽  
Vol 105 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Aránzazu URUÑUELA ◽  
Manuel A. MANSO ◽  
Ana M. DE LA MANO ◽  
Isabel DE DIOS

Cholecystokinin (CCK) has been suggested to be a contributory mediator in acute pancreatitis (AP). The aim of the present study was to assess the role of CCK in the development of oxidative stress at different stages of AP induced by pancreatic duct obstruction (PDO) in rats, using L364,718 (a potent CCK-receptor antagonist) to block CCK action. Intra-acinar oxygen free radical (OFR) generation was analysed by flow cytometry using dihydrorhodamine-123 as a fluorogenic dye. Parallel measurements of pancreatic levels of reduced glutathione (GSH) and of several parameters for the diagnosis of AP were performed in both untreated PDO rats and PDO rats receiving L364,718 (0.1 mg·12 h-1·kg-1). Diagnosis parameters indicated a greater severity of AP in rats treated with the CCK antagonist. The increase in OFR generation observed in acinar cells up to 12 h after inducing AP was triggered at an earlier stages and reached higher values when L364,718 was administered. Accordingly, greater pancreatic GSH depletion was observed in rats with AP treated with the CCK antagonist. Two populations of acinar cells that were differentiated by flow cytometry, R1 and R2, showed similar behaviour with regard to OFR generation in PDO rats; however, R1 cells showed greater sensitivity to L364,718 administration, and thus OFR production was increased in R1 cells earlier than in R2 cells. In conclusion, CCK blockade anticipates and enhances the amount of OFR produced in acinar cells as a consequence of AP, thus leading to earlier development of and more severe disease. The detrimental effect of L364,718 in AP induced by PDO suggests that plasma CCK does not play a major role in the development of this AP model.


2004 ◽  
Vol 51 (1-2) ◽  
pp. 70-75 ◽  
Author(s):  
Miho Kurahashi ◽  
Hidenori Miyake ◽  
Toshihide Takagi ◽  
Seiki Tashiro

2003 ◽  
Vol 278 (17) ◽  
pp. 15456
Author(s):  
Frank Ch. Mooren ◽  
Verena Hlouschek ◽  
Till Finkes ◽  
Stefan Turi ◽  
Ina Alexandra Weber ◽  
...  

2020 ◽  
Vol 08 (12) ◽  
pp. E1765-E1768
Author(s):  
Ryoko Shimizuguchi ◽  
Masataka Kikuyama ◽  
Terumi Kamisawa ◽  
Sawako Kuruma ◽  
Kazuro Chiba

Abstract Background and study aims Acute obstructive suppurative pancreatic ductitis (AOSPD) is a suppurative pancreatic duct infection with main pancreatic duct (MPD) or accessory pancreatic duct obstruction in the absence of a pancreatic pseudocyst or necrosis, which is experienced usually in chronic pancreatitis. The diagnosis is confirmed by the finding of pancreatic duct obstruction on endoscopic retrograde cholangiopancreatography (ERCP) with evidence of infection, such as a positive pancreatic juice culture or drainage of purulent pancreatic juice. Patients and methods We studied five patients with pancreatic ductal adenocarcinoma (PDAC) and one with chronic myelogenous leukemia (CML), who suffered from AOSPD. Results Of the 281 PDAC and 39 CML patients who we treated in the past 2 years in our hospital, five with PDAC (1.8 %) and one with CML (2.6 %) experienced AOSPD. Each patient had fever, abdominal pain, and increased blood C-reactive protein. Pancreatography found that each patient had a MPD stricture and an upstream dilatation. Four had a disruption of the MPD in the upper stream of the stricture. Nasopancreatic drainage was successfully performed in all patients. Pancreatic juice culture was positive for Klebsiella pneumonia, Enterobacter agerogenes, or Enterococcus cloacae in four patients. Conclusion AOSPD should be considered in pancreatic malignancy with fever and abdominal pain. Prompt diagnosis of AOSPD could avoid shortening of survival of patients with an already poor prognosis by infection.


1976 ◽  
Vol 132 (5) ◽  
pp. 662-663 ◽  
Author(s):  
Kunio Ohmori ◽  
Hiroaki Kinoshita ◽  
Yaemon Shiraha ◽  
Katsusuke Satake

1991 ◽  
Vol 100 (1) ◽  
pp. 196-202 ◽  
Author(s):  
G. Ohshio ◽  
A. Saluja ◽  
M.L. Steer

1996 ◽  
Vol 41 (10) ◽  
pp. 1947-1952 ◽  
Author(s):  
Gakuji Ohshio ◽  
Toshirou Tanaka ◽  
Takashi Imamura ◽  
Noriyuki Okada ◽  
Shouichi Yoshitomi ◽  
...  

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