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

Nitric oxide (NO) as a unique biologicalmediator that has been implicated i n many physiological and pathophysiological processes may have a significan t influence on the course of acute pancreatitis and the recovery process. T he aim of the study was to evaluate the effect of a NO synthase inhibitor o r 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 caerul ein, During acute pancreatitis induction, the rats were treated with L-argi nine (the substrate for NO synthesis), N-G-nitro-L-arginine (L-NNA, NO synt hase inhibitor), L-arginine + L-NNA or saline. Light and electron microscop y examinations were performed in all groups after pancreatitis induction an d additionally after 7 and 14 days of recovery. The study demonstrated that the NO synthase inhibitor given during pancreatitis induction in rats enha nces the damage to the acinar cells, detected ultrastructurally, and increa ses the cellular inflammatory infiltration. In the later period, the consid erable damage to the mitochondria and the changes in secretory compartment were observed, including dilated cisternae of Golgi apparatus, focal degran ulation of rough endoplasmic reticulum, and reduced number of zymogen granu les and condensing vacuoles. L-arginine reversed to some extent the deleter ious effect of L-NNA, although when administered alone it had no apparent e ffect on the ultrastructure of pancreatic acinar cells compared with untrea ted animals. The obtained results indicate that the NO synthase inhibitor e nhances the ultrastructural degenerative alterations in the pancreatic acin ar cells in the course of caerulein-induced acute pancreatitis and confirm the protective role of endogenous nitric oxide in this disease.