Abstract
Chronic pancreatitis is thought to be incurable. However, we suspected that the pancreas regenerates in cases of chronic pancreatitis. We examined the histological features of chronic pancreatitis mainly in surgically removed human specimens. Morphologically, regenerated pancreas was compared between experimental pancreas and human pancreas. To cause experimental pancreatitis, dl-ethionine, which is an antagonist of methionine, was used. Pathological similarities in human chronic pancreatitis and experimental pancreatitis were compared. The experimental animals comprised rats and dogs. Rats were principally used for studies on the phenomenon of destruction and regeneration in the pancreas. Dogs were used in the experimental study of chronic pancreatitis, and to assess quantitative changes of fibrous tissue and experimental regeneration of the pancreas. Experimentally, the damaged pancreas was examined immuno-histologically. Also, the influence of trypsin inhibitor during pancreatic regeneration was examined by BrdU. Quantitative changes of the fibrous tissue appeared after the destruction of the pancreas. The purpose of experiments was to elucidate the cause of the regeneration of chronic pancreatitis. In experimental pancreatitis, atrophy of the pancreas and the increase of fibrous tissue were almost similar to human chronic pancreatitis. A large quantity of fiber seen in human chronic pancreatitis reacted to α smooth muscle actin strongly. The factor that has been considered to disturb the regeneration of the pancreas is the myofibroblast, which is a subspecies of the fibroblast. In experimental pancreatitis, it was thought that a substance acting between acinar cells controls the amount of fibrous tissue in the pancreas. In addition, it was thought that myofibroblasts produce various mediators. It is suggested that an increase of myofibroblasts suppresses the regeneration of the pancreas in chronic pancreatitis.
