Uchida T, Tsuchiya R, Harada N, Tsunoda T, Yamaguchi T, Eto T, Furukawa M
Second Department of Surgery, Nagasaki University School of Medicine, Japan.
Int J Pancreatol. 1988 May;3(4):261-71. doi: 10.1007/BF02788455.
Arterial intimal thickening and thrombosis of the pancreatic artery has frequently been found in Watanabe heritable hyper-lipidemic (WHHL) rabbits. Three of the 20 rabbits used in this study showed histopathological findings such as intra- or inter-lobular fibrosis with lymphocytic infiltration, acinar degenerative changes, ductular proliferation and small ductal dilatations which were identical to those of human chronic pancreatitis. These findings were observed in discrete areas clearly demarcated from normal pancreatic parenchyma and adjacent to parenchymal necrosis. These discrete areas were developed just peripheral to regions of necrotic or inflammatory obstruction of the pancreatic duct, which might have been caused by parenchymal necrosis due to severe ischemia. The stasis of pancreatic juice in the ductal tree may result in such findings in the WHHL rabbit. Fat replacement of pancreatic parenchyma was observed in 17 of the 20 WHHL rabbits, and was classified into two types, diffuse and massive. Massive fat replacement may occur from fat necrosis and intra-lobular parenchymal necrosis. Vascular alterations and secondary ischemia in the pancreas is one of the most important factors involved in the pancreatic lesions present in the WHHL rabbit.