The role of nitric oxide in caerulein-induced acute pancreatitis and the recovery process after inflammatory damage

Citation
G. Jurkowska et al., The role of nitric oxide in caerulein-induced acute pancreatitis and the recovery process after inflammatory damage, EUR J GASTR, 11(9), 1999, pp. 1019-1026
Citations number
41
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
ISSN journal
0954691X → ACNP
Volume
11
Issue
9
Year of publication
1999
Pages
1019 - 1026
Database
ISI
SICI code
0954-691X(199909)11:9<1019:TRONOI>2.0.ZU;2-#
Abstract
Objectives Nitric oxide (NO) is involved in the control of pancreatic blood flow and secretion, and its role in the maintenance of pancreatic tissue h as been suggested. The aim of our study was to evaluate the influence of NO on pancreatic trophic parameters during acute pancreatitis induction and t he pancreas recovery process. Design/methods Acute pancreatitis was induced in rats by a supramaximal dos e of caerulein. During acute pancreatitis induction, rats were treated with L-arginine (a substrate for NO synthesis), glyceryl trinitrate (NTG, NO do nor), glycine, NG-nitro-L-arginine (L-NNA, NO synthase inhibitor), L-argini ne + L-NNA, or saline. Pancreatic weight, total contents of RNA, DNA, prote in, amylase and chymotrypsin as well as pancreas histology and the number o f proliferating acinar cells were evaluated after pancreatitis induction in all groups and additionally after 7 and 14 days of recovery in untreated a cute pancreatitis rats or those injected with L-NNA and/or L-arginine. Results Pancreas destruction after acute pancreatitis was evidenced by simi lar decreases of all parameters in untreated acute pancreatitis rats or tho se treated with L-NNA or glycine when compared to control healthy animals. The recovery process after acute pancreatitis was not affected by L-NNA inj ections; however, the increased cell proliferation occurred later than in u ntreated rats. NTG and especially L-arginine treatment resulted in signific ant attenuation of pancreas damage (partially prevented by L-NNA treatment) as evidenced by biochemical data with a slight improvement in morphology. Treatment with L-arginine alone or in combination with L-NNA resulted in au gmented cell proliferation after acute pancreatitis induction followed by e arlier recovery in comparison to untreated acute pancreatitis rats or the L -NNA-injected group. Conclusion The present study suggests the involvement of NO in mild acute p ancreatitis and in the recovery process after inflammatory damage. Eur J Ga stroenterol Hepatol 11:1019-1026 (C) 1999 Lippincott Williams & Wilkins.