[Pathophysiologic concepts and protective possibilities in experimental pancreatic lesions].
Experimental pancreatic lesions can be induced by a number of different procedures, e.g. pancreatic hyperstimulation, intraductal application of bile acids, feeding choline deficient diet, obstruction of pancreatic duct, or reducing pancreatic blood flow. The pathogenetic mechanisms leading to pancreatic lesions include basolateral enzyme secretion, acinar cell polarisation defect, intracellular activation of proteases, and the production of free radicals and other active metabolites. The importance of these individual mechanisms in the production and progression of different experimentally-induced pancreatic lesions remains speculative. These pathogenetic concepts have inspired the study of a number of substances likely to protect the pancreas and prevent the pancreatic lesions. This paper gives an overview of the pathogenetic concepts of development of and protection against experimental pancreatic lesions produced in animal models. Special mention has been made of an animal model of pancreatic lesion produced by immunosuppressives.
Müller
M K
MK
Medizinische Klinik IV-Gastroenterologie, Klinikum Mannheim, Universität Heidelberg.
Keim
V
V
Chari
S
S
D000818:Animals; D016572:Cyclosporine; D010179:Pancreas / Q000503:physiopathology; D010195:Pancreatitis / Q000139:chemically induced / Q000503:physiopathology* / Q000517:prevention & control; D017382:Reactive Oxygen Species / Q000378:metabolism; D016559:Tacrolimus
D017382:Reactive Oxygen Species; D016572:Cyclosporine; D016559:Tacrolimus