Many experimental models have been created to explain the pathophysiology
of acute pancreatitis (AP). Investigations have been undertaken in this laboratory
into the influence of strong oxidants introduced into the pancreas retrogradely
through the bile-pancreatic duct. In these experiments a potentially toxic
metabolite of ethanol-peracetic acid was used to induce AP. Wistar rats were
treated with 1 mM and 40 mM peracetate and with a solvent as a control for
1 and 3 hours respectively. After a period of observation the samples of pancreata
were examined in a light and electron microscope together with the content
of sulphydryl groups as a marker of intracellular oxidative stress. The morphological
examination showed profound changes in the histology of the pancreas
and also in its subcellular structures, especially in groups 3 and 4 (with a higher
concentration of peracetate). The changes included parenchymal haemorrhage
and widespread acinar cell necrosis. The level of the sulphydryl groups decreased
in the rats treated with peracetate. This suggests that the severity of the disease
strongly depends on the intensity of the oxidative stress. The results confirmed
the axial role of oxygen-derived free radicals in the pathogenesis of AP