OBJECTIVES: We developed a new model of reversible pancreatitis, as an incomplete closed duodenal loop (ICDL) model. This permitted us to demonstrate the process of progressing severity of pancreatitis and the influence of tissue microcirculation impairment on the morphologic changes of pancreatitis. METHODS: An ICDL model was prepared in Wistar rats according to the following procedure. The duodenum was ligated over half its circumference at 2 cm on either side of the duodenal entry of the biliopancreatic duct. RESULTS: The pancreatic wet weight ratio in the ICDL was higher than that of the control after model preparation. The survival rate in the ICDL group was significantly longer than that in the CDL group. Blood flow in the pancreas and duodenal loop decreased over time after model preparation, and the decline in ICDL occurred and remained at a plateau in chronic pancreatitis phase. Histopathologic alterations of the pancreas in the ICDL group consisted of edema, parenchymal necrosis, thrombosis, and hemorrhage. From 1 week onward, periductal fibrosis spread to the parenchyma, the regenerative activity of the acinar cell presenting the clinical features of chronic pancreatitis. CONCLUSION: Impairment of microcirculation due to tissue ischemia played a role in the increasing severity of pancreatitis.
OBJECTIVES: We developed a new model of reversible pancreatitis, as an incomplete closed duodenal loop (ICDL) model. This permitted us to demonstrate the process of progressing severity of pancreatitis and the influence of tissue microcirculation impairment on the morphologic changes of pancreatitis. METHODS: An ICDL model was prepared in Wistar rats according to the following procedure. The duodenum was ligated over half its circumference at 2 cm on either side of the duodenal entry of the biliopancreatic duct. RESULTS: The pancreatic wet weight ratio in the ICDL was higher than that of the control after model preparation. The survival rate in the ICDL group was significantly longer than that in the CDL group. Blood flow in the pancreas and duodenal loop decreased over time after model preparation, and the decline in ICDL occurred and remained at a plateau in chronic pancreatitis phase. Histopathologic alterations of the pancreas in the ICDL group consisted of edema, parenchymal necrosis, thrombosis, and hemorrhage. From 1 week onward, periductal fibrosis spread to the parenchyma, the regenerative activity of the acinar cell presenting the clinical features of chronic pancreatitis. CONCLUSION: Impairment of microcirculation due to tissue ischemia played a role in the increasing severity of pancreatitis.
Authors: Kathryn M Ziegler; Terence E Wade; Sue Wang; Deborah A Swartz-Basile; Henry A Pitt; Nicholas J Zyromski Journal: Am J Transl Res Date: 2010-12-23 Impact factor: 4.060
Authors: Pedro Silva-Vaz; Ana Margarida Abrantes; Miguel Castelo-Branco; António Gouveia; Maria Filomena Botelho; José Guilherme Tralhão Journal: Int J Mol Sci Date: 2019-06-07 Impact factor: 5.923