Nitric oxide protects the ultrastructure of pancreatic acinar cells in the course of caerulein-induced acute pancreatitis

• Published in: International journal of experimental pathology Vol. 80; no. 6; pp. 317 - 324
• Main Authors: Andrzejewska, Anna, Jurkowska, Grazyna
• Format: Journal Article
• Language: English
• Published: Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 01.12.1999; Blackwell Science; Blackwell Science Inc
• Subjects: Acute Disease; acute pancreatitis; Animals; Arginine - pharmacology; Biological and medical sciences; Ceruletide; Enzyme Inhibitors - pharmacology; Gastroenterology. Liver. Pancreas. Abdomen; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Male; Medical sciences; Microscopy, Electron; nitric oxide; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; Nitroarginine - pharmacology; Original; Other diseases. Semiology; Pancreas - drug effects; Pancreas - ultrastructure; Pancreatitis - chemically induced; Pancreatitis - pathology; Pancreatitis - physiopathology; Rats; Rats, Wistar; ultrastructure; Rat; Acute; Rodentia; Pancreatitis; Cerulein; Electron microscopy; Pathology; Vertebrata; Optical microscopy; Experimental disease; Mammalia; Animal; Nitric oxide; Digestive diseases; Protection; Pancreatic disease
• ISSN: 0959-9673; 1365-2613
• DOI: 10.1046/j.1365-2613.1999.00126.x

Nitric oxide (NO) as a unique biologicalmediator that has been implicated in many physiological and pathophysiological processes may have a significant influence on the course of acute pancreatitis and the recovery process. The aim of the study was to evaluate the effect of a NO synthase inhibitor or a substrate for NO endogenous production on the ultrastructural features of the acinar cells in the course of caerulein‐induced acute pancreatitis. Acute pancreatitis was induced in the rats by a supramaximal dose of caerulein. During acute pancreatitis induction, the rats were treated with l‐arginine (the substrate for NO synthesis), NG‐nitro‐ l‐arginine (L‐NNA, NO synthase inhibitor), l‐arginine + L‐NNA or saline. Light and electron microscopy examinations were performed in all groups after pancreatitis induction and additionally after 7 and 14 days of recovery. The study demonstrated that the NO synthase inhibitor given during pancreatitis induction in rats enhances the damage to the acinar cells, detected ultrastructurally, and increases the cellular inflammatory infiltration. In the later period, the considerable damage to the mitochondria and the changes in secretory compartment were observed, including dilated cisternae of Golgi apparatus, focal degranulation of rough endoplasmic reticulum, and reduced number of zymogen granules and condensing vacuoles. l‐arginine reversed to some extent the deleterious effect of L‐NNA, although when administered alone it had no apparent effect on the ultrastructure of pancreatic acinar cells compared with untreated animals. The obtained results indicate that the NO synthase inhibitor enhances the ultrastructural degenerative alterations in the pancreatic acinar cells in the course of caerulein‐induced acute pancreatitis and confirm the protective role of endogenous nitric oxide in this disease.