[The role of glucocorticoid-dependent mechanisms in the progression of experimentally induced acute pancreatitis]

Magy Seb. 2003 Oct;56(5):185-92.
[Article in Hungarian]

Abstract

Background: The effects of glucocorticoids on acute pancreatitis (AP) have remained contradictory. To investigate the time courses of the effects of the exogenous glucocorticoid agonists dexamethasone (DEX) and hydrocortisone (HYD) and a glucocorticoid antagonist (RU-38486), and to characterize the local and systemic responses in experimental AP.

Methods: The glucocorticoid agonists and antagonist were administered just before AP induction. Serum amylase activity determinations, IL-6 bioassays, pancreatic weight/body weight ratio measurements and survival analysis were performed. Liver and lung injuries were assessed via neutrophil leukocyte infiltration in myeloperoxidase (MPO) assays, tissue adenosine triphosphate (ATP) level determinations and histology.

Results: In the glucocorticoid agonist groups, the survival rate increased, while the serum amylase level, the IL-6 activity and the pancreatic weight/body weight ratio decreased significantly as compared with the control and RU-treated groups. AP resulted in significant decreases in tissue ATP levels in both the liver and the lung. In the DEX- or HYD-treated groups, the liver ATP levels were significantly elevated, while both the liver and the lung MPO levels were attenuated as compared with the AP and RU-treated groups.

Conclusions: These results suggest that glucocorticoids may play important roles in mitigating the progression of the inflammatory reaction during the early phases of AP.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Adenosine Triphosphate / metabolism
  • Amylases / blood
  • Animals
  • Body Weight
  • Clinical Enzyme Tests
  • Glucocorticoids / metabolism*
  • Interleukin-6 / blood
  • Liver / pathology
  • Lung / pathology
  • Multiple Organ Failure / metabolism
  • Neutrophils
  • Organ Size
  • Pancreatitis / enzymology
  • Pancreatitis / metabolism*
  • Pancreatitis / pathology
  • Pancreatitis / physiopathology
  • Peroxidase / metabolism
  • Rats
  • Rats, Wistar

Substances

  • Glucocorticoids
  • Interleukin-6
  • Adenosine Triphosphate
  • Peroxidase
  • Amylases