Acute edematous and necrotic pancreatitis in a porcine model

It is unclear why pancreatitis progresses either to mild edematous disease or to severe necrotic disease. The aim of the study was to shed some light on this topic by investigating differences during the early stages of necrotic and edematous pancreatitis.

Piglets were randomized into two groups. Necrotic pancreatitis was induced with retrograde injection of 20% taurocholic acid (1 ml/kg), and edematous pancreatitis was induced with 0.9% NaCl (1 ml/kg). Central hemodynamics was measured, and pancreatic microcirculation was directly examined by intravital microscopy. Vascular permeability to proteins and albumin was measured by microdialysis. Apoptosis and claudins 2, 3, 4, 5, and 7 were analyzed from pancreatic tissue samples. Blood samples were taken for analysis of blood cell counts, blood gases, lipase, and amylase.

Hemodynamic changes were similar in both groups, whereas microcirculatory impairment was more pronounced in necrotic pancreatitis. Necrosis was associated only with necrotic pancreatitis. Apoptosis increased only in edematous pancreatitis. The number of blood neutrophils and monocytes increased and lymphocyte and platelet counts decreased in both groups. Necrotic pancreatitis was associated with increased permeability to albumin and proteins. Expression of claudins 3, 4, 5, and 7 was not changed during pacreatitis, but in acinar cells, membranous expression of claudin-2 increased in both groups.

The results show that acute edematous pancreatitis is characterized by induction of apoptosis, whereas full-blown pancreatitis is characterized by necrosis. Impaired vascular permeability to albumin and protein is related to the early phase of necrotic pancreatitis. Claudin-2 increases during acute necrotic and edematous pancreatitis and may be related to impaired permeability.