Studies on serum immunoreactive elastase in experimental pancreatitis rats I. in acute pancreatitis

1980 ◽  
Vol 15 (6) ◽  
pp. 620-624 ◽  
Author(s):  
Toshinari Kimura ◽  
Kouichiro Imamura ◽  
Masahiro Matsumoto ◽  
Hideyuki Wakasugi ◽  
Hiroshi Ibayashi
1991 ◽  
Vol 261 (3) ◽  
pp. G485-G489 ◽  
Author(s):  
J. L. Iovanna ◽  
V. Keim ◽  
R. Michel ◽  
J. C. Dagorn

We investigated pancreatic gene expression in the rat in response to taurocholate-induced acute pancreatitis. Concentrations of transcripts encoding pancreatic protein showed noncoordinated alterations. Contents in amylase, trypsinogen I, chymotrypsinogen B, elastase 1, and procarboxypeptidase A mRNAs decreased by greater than 50% during the acute phase (days 0-2), whereas actin and lithostathine mRNAs increased 5 and 0.6 times, respectively, and pancreatitis-associated protein (PAP) mRNA increased greater than 200 times, indicating redirection of the pattern of gene expression. Synthesis of pancreatic proteins was also altered in a noncoordinated manner. During the acute phase, it decreased more for trypsinogen I and chymotrypsinogen B than for amylase and lipase, whereas synthesis of the PAP increased dramatically. For amylase and chymotrypsinogen B, we compared the patterns of changes in mRNA concentrations, rates of synthesis, and pancreatic contents. Changes in enzyme contents and synthetic rates were temporally correlated during the acute phase. On the contrary, changes in mRNA concentrations and enzyme synthesis were not coordinated, suggesting that control of synthesis partly occurred at the posttranscriptional level. It was concluded that induction of pancreatitis is accompanied by transcriptional and posttranscriptional modifications resulting in rapid and massive rearrangement of the pattern of pancreatic protein gene expression.


2019 ◽  
Vol 70 (2) ◽  
pp. 676-678
Author(s):  
Alexandru Grigorovici ◽  
cristian Velicescu ◽  
Delia Hinganu ◽  
Alina Calin ◽  
Marius Valeriu Hinganu ◽  
...  

The concept of chronic pancreatitis has been stated in our country much later than acute pancreatitis. This manuscript proposes a synthesis of the etiopathogenic, diagnostic and therapeutic data in chronic pancreatitis based on actual information correlated with the results of our experimental study. The experiment was conducted on 18 animals, in which was performed the intraduodenal ligation of the pancreatic duct apertures and the obstruction of the pancreatic ducts with intraparenchymatous, intraoperative neoprene injections. We investigated the lesions by using intraoperative pancreatic tissue collected after injections. The results encourage us to continue the research and to choose genetically modified animals because are closer to the human one.


2007 ◽  
Vol 292 (6) ◽  
pp. G1738-G1746 ◽  
Author(s):  
Gijs J. D. Van Acker ◽  
Eric Weiss ◽  
Michael L. Steer ◽  
George Perides

We have hypothesized that the colocalization of digestive zymogens with lysosomal hydrolases, which occurs during the early stages of every experimental pancreatitis model, facilitates activation of those zymogens by lysosomal hydrolases such as cathepsin B and that this activation triggers acute pancreatitis by leading to acinar cell injury. Some, however, have argued that the colocalization phenomenon may be the result, rather than the cause, of zymogen activation during pancreatitis. To resolve this controversy and explore the causal relationships between zymogen activation and other early pancreatitis events, we induced pancreatitis in mice by repeated supramaximal secretagogue stimulation with caerulein. Some animals were pretreated with the cathepsin B inhibitor CA-074me to inhibit cathepsin B, prevent intrapancreatic activation of digestive zymogens, and reduce the severity of pancreatitis. We show that inhibition of cathepsin B by pretreatment with CA-074me prevents intrapancreatic zymogen activation and reduces organellar fragility, but it does not alter the caerulein-induced colocalization phenomenon or subcellular F-actin redistribution or prevent caerulein-induced activation of NF-κB, ERK1/2, and JNK or upregulated expression of cytochemokines. We conclude 1) that the colocalization phenomenon, F-actin redistribution, activation of proinflammatory transcription factors, and upregulated expression of cytochemokines are not the results of zymogen activation, and 2) that these early events in pancreatitis are not dependent on cathepsin B activity. In contrast, zymogen activation and increased subcellular organellar fragility during caerulein-induced pancreatitis are dependent on cathepsin B activity.


2008 ◽  
Vol 52 (4) ◽  
pp. 1516-1518 ◽  
Author(s):  
Sandrine Lefeuvre ◽  
Sandrine Marchand ◽  
Claudine Pariat ◽  
Isabelle Lamarche ◽  
William Couet

ABSTRACT Imipenem distribution was characterized by microdialysis in the peritoneal fluid of rats with experimental pancreatitis. The ratios of peritoneal fluid to blood area under unbound concentration-versus-time curves were close to unity, suggesting that imipenem was not degraded in peritoneal fluid.


1971 ◽  
Vol 3 (1) ◽  
pp. 31-42 ◽  
Author(s):  
Hooshang Bolooki ◽  
Stanley Minkowitz ◽  
Samuel T. Giammona ◽  
James R. Jude

Sign in / Sign up

Export Citation Format

Share Document