The influence of nitric oxide synthesis modulation on the pancreatic acinar cells in caerulein-induced acute pancreatitis. An ultrastructural and morphometric study.

The goal of our study was to evaluate the influence of NO synthesis modulation on the ultrastructural changes in the pancreatic acinar cells in connection with morphometric assessment of the volume and numerical densities of mitochondria (Vvm, Nvm) and zymogen granules (Vvz, Nvz) in caerulein-induced acute pancreatitis (AP). During AP induction rats were treated with L-arginine--substrate for NO synthesis, N(G)-nitro-L-arginine (L-NNA)--NO synthase inhibitor, gliceryl trinitrate (NTG)--NO donor, L-arginine+L-NNA or saline. This study demonstrated that administration of L-NNA leads to the formation of numerous, large autophagosomes and mitochondria oedema in pancreatic acinar cells. Treatment with L-arginine or NTG during AP induction resulted in a diminution of the ultrastructural changes with a concomitant increase of Vvz. Vvm and Nvm were significantly lower in the L-arginine treated group compared to the untreated AP. The results indicate that: L-NNA enhances damage to acinar cells which may be indicative of a protective role for endogenous NO in oedematous AP. The application of L-arginine or NTG decreases the damage to acinar cells evaluated ultrastructurally, suggesting the morphological changes accompanying the onset of AP in rats after the administration of either substrate for endogenous NO synthesis or exogenous NO donor follow a favourable course.