Pathomorphological analysis of the pancreaticoduodenal organs in experimental pancreonecrosis induced by trypsin injection.

Acute experimental pancreatitis induced by injection of trypsin into the pancreatic tissue exhibited characteristics of fulminant hemorrhagic pancreonecrosis (intense exudation of interlobular stroma, massive plasmo- and hemorrhages, foci of acinar cell autolysis involving by the end of day 1 an appreciable portion of the organ with formation of fields of necrosis and hemorrhagic imbibition of the glandular parenchyma, virtually completely without demarcation cellular reaction). Marked microcirculatory disorders and degenerative and necrobiotic changes in the duodenal mucosa and liver reflected the polyorgan nature of the pathological process. This model of hemorrhagic pancreonecrosis corresponded to the most severe forms of this conditions observed clinically.

Pancreatic fat necrosis and hemorrhagic necrosis as separate morphological and functional entities.

Peculiarities of pathomorphogenesis of two destructive forms of acute pancreatitis were compared using three experimental models. We have shown that the direction of the pathological process is determined by specific combinations of pathogenic factors. Pathological processes caused by common bile duct ligation (ductal hypertension) alone and in combination with injection of phospholipase A2 are characterized by mixed pattern with strong predominance of fat necrosis symptoms (coagulative acinar necrosis, inflammatory demarcation, and sites of lipolysis) and hemorrhagic necrosis, respectively. Trypsin injection into the pancreatic tissue induces rapidly progressing hemorrhagic pancreatic necrosis with massive hemorrhages, extensive acinar necrosis, and weak cell reaction. Considerable differences in pathomorphogenesis and outcome of the pathological process allow us to consider pancreatic fat necrosis and hemorrhagic necrosis as separate morphological and functional entities, which is essential for the prognosis and treatment strategy.

[Pathogenetic aspects of proteolysis and hemorrhagic pancreatonecrosis and methods of their correction].

In the work you can find the results of the research on modeling of acute experimental pancreatitis caused by injecting solution of tripsin and vipera berus venom. All the visceral organs are involved, that corresponds to common to the human and animal pathological processes (induction of proteolysis and DIC-syndrome). The results of the research show and prove the effectiveness of sandostatin and anti-ophidic serum influence on the proteolytic processes, blood coagulation. Thus, this research gives the opportunity to possibly expand the usage of sandostatin and anti-ophidic serum on treatment diseases with the participation of cascade proteolytic processes.

[Pathomorphological changes in the pancreatic ductal system in fatty and hemorrhagic pancreonecrosis in experiment].

The pancreatic ductal system was morphologically studied in fatty and hemorrhagic pancreonecrosis in experiments. The latter were carried out on 105 male Wistar rats. The use of the study models of fatty (administration of phospholipase A2, common bile duct ligation, and their combination) and hemorrhagic pancreonecrosis (administration of trypsin and snake venom) has shown that in fatty pancreonecrosis there are changes initially revealed in the pancreatic ductal system with subsequent necrosis of its parenchyma. In hemorrhagic pancreonecrosis, the ductal system retains its structure. Based on the findings, the authors soundly identify two forms of acute pancreatitis: primary acinar (parenchymatous) and hypertensive ductal.

Pathomorphological study of the pancreas during phospholipase A2-induced experimental pancreatic necrosis.

The pathomorphogenesis of experimental acute pancreatic necrosis induced by administration of phospholipase A2 into the pancreatic tissue is characterized by pathomorphological signs of hemorrhagic pancreatic necrosis (total necrosis and purulent fusion of some acini and massive hemorrhages in the interlobular and intralobular interstitial tissue) and fatty pancreatic necrosis (necrobiotic and necrotic changes in acinar cells that spread from the peripheral area and form the demarcation line).

Ultrastructure of acinar cell injuries in experimental acute pancreatitis created by common bile duct ligation.

Morphogenesis of acute pancreatitis induced by ligation of the common bile duct and the ultrastructure of autolytic transformations of acinar cells were studied. Autolytic changes in acinar cells started from the basal zones and then involved the apical zones. Violation of the zymogen granules integrity, interactions of their contents with the adjacent ultrastructures, destruction (melting) of ultrastructures, and formation of huge autophagosomes play an important role in the development of autolysis. Disordered secretion of zymogen granules (foci of their accumulation in the apical zone), hyperplasia and hypertrophy of centroacinar cells and ductal epitheliocytes aimed at restoration of the pancreatic secretion discharge pathways were seen in the retained acini.