Abstract
Using a guinea pig model, we examined the mechanism of cell loss in experimental pancreatitis by immunohistochemistry and electron microscopy. Acinar cells in pancreatitis foci were completely deleted by one week, and proliferation of pancreatic ductuli appeared at three days, increased by two weeks, and then decreased by six months. Approximately 30% of acinar cells in the pancreatitis foci were positive with TUNEL immunohistochemistry at three days. By one week, numbers of positive cells had decreased. TUNEL-positive ductular cells appeared at three days, increased by two weeks, and then gradually decreased by three months. At three days, most acinar cells showed necrotic change by electron microscopy, with some cells undergoing apoptosis. Proliferated ductular cells did not show necrotic change, but were undergoing apoptosis continuously from one week to six months, therefore apoptosis does participate in the course of ductular deletion. As apoptosis is a mechanism of silent cell death carrying no inflammatory aggregates, it should be favorable for pancreatic ductuli to be deleted by apoptosis in the healing state of pancreatitis. It is concluded that apoptosis, rather than acinar cell loss, plays a major role in subsequent loss of proliferated pancreatic ductuli in experimental pancreatitis.
