Kinetic study of TNF-α production and its regulatory mechanisms in acinar cells during acute pancreatitis induced by bile–pancreatic duct obstruction

2005 ◽  
Vol 206 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Laura Ramudo ◽  
Manuel A Manso ◽  
Sara Sevillano ◽  
Isabel de Dios
Keyword(s):  
Acute Pancreatitis ◽  
Kinetic Study ◽  
Pancreatic Duct ◽  
Acinar Cells ◽  
Regulatory Mechanisms ◽  
Duct Obstruction ◽  
Pancreatic Duct Obstruction ◽  
Tnf Α

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

2002 ◽  
Vol 102 (6) ◽  
pp. 615-622 ◽  
Author(s):  
Aránzazu URUÑUELA ◽  
Manuel A. MANSO ◽  
Ana Ma DE LA MANO ◽  
Sara SEVILLANO ◽  
Alberto ORFAO ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Acute Pancreatitis ◽  
Pancreatic Duct ◽  
Basolateral Membrane ◽  
Acinar Cells ◽  
Current Evidence ◽  
Duct Obstruction ◽  
Morphological Alterations ◽  
Pancreatic Duct Obstruction ◽  
Severity Of The Disease

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.

Cholecystokinin blockade triggers earlier and enhanced intra-acinar oxygen free radical generation in acute pancreatitis induced by pancreatic duct obstruction in rats

2003 ◽  
Vol 105 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Aránzazu URUÑUELA ◽  
Manuel A. MANSO ◽  
Ana M. DE LA MANO ◽  
Isabel DE DIOS
Keyword(s):  
Flow Cytometry ◽  
Acute Pancreatitis ◽  
Free Radical ◽  
Pancreatic Duct ◽  
Severe Disease ◽  
Acinar Cells ◽  
Oxygen Free Radical ◽  
Duct Obstruction ◽  
Pancreatic Duct Obstruction ◽  
Cck Antagonist

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.

Effect of dexamethasone on peripheral blood leukocyte immune response in bile-pancreatic duct obstruction-induced acute pancreatitis

Steroids ◽  
2010 ◽  
Vol 75 (4-5) ◽  
pp. 362-367 ◽  
Author(s):  
Laura Ramudo ◽  
Sara Yubero ◽  
Manuel A. Manso ◽  
Javier S. Recio ◽  
Eduardo Weruaga ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Pancreatitis ◽  
Pancreatic Duct ◽  
Peripheral Blood ◽  
Peripheral Blood Leukocyte ◽  
Duct Obstruction ◽  
Pancreatic Duct Obstruction ◽  
Blood Leukocyte

Bile Exclusion from the Gut Exacerbates Acute Pancreatitis Caused by Pancreatic Duct Obstruction in Rats

Pancreas ◽  
1991 ◽  
Vol 6 (2) ◽  
pp. 175-181 ◽  
Author(s):  
Kenric M. Murayama ◽  
James B. Drew ◽  
Hidejiro Yokoo ◽  
Raymond J. Joehl
Keyword(s):  
Acute Pancreatitis ◽  
Pancreatic Duct ◽  
Duct Obstruction ◽  
Pancreatic Duct Obstruction

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 ◽  
...  
Keyword(s):  
Pancreatic Duct ◽  
Acinar Cells ◽  
Duct Obstruction ◽  
Pancreatic Duct Obstruction
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