Involvement of Oxidative Stress in Sodium Taurocholate-Induced Acute Necrotizing Pancreatitis in Rats

Oxidative radicals are regarded as a major factor in the pathogenesis of both acute and chronic pancreatitis. Because oxygen radicals react most readily with polyunsaturated fatty acids, resulting in peroxidation of lipids, several studies have been performed to determine the development of lipid peroxidation in pancreatitis. The purpose of this study was to evaluate the effects of free radicals and decision of the experimental model in acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 18 rats by retrograde injection into the bilopancreatic duct of 2%, 3%, and 5% sodium taurocholate. After a 12-hour observation time, the pancreas / the body weight, the serum amylase and the malondialdehyde content in tissue, as well as the reduced glutathione were measured in resected tissue samples. In addition, to determine the pathologic damage grade, tissue samples were examined by light microscopy. According to the amount of sodium taurocholate injected, the serum amylase and tissue malondialdehyde concentration were significantly increased. The reduced glutathione was significantly decreased, suggesting glutathione depletion due to oxidative stress. During the 12 hours after injection the pancreatic lesions were immediate and were characterized by interstitial edema, atrophy and extensive necrotic changes of the acinar cells, and hemorrhage. The pathologic damage grade increased according to the amount of sodium taurocholate injected. This study created an experimental model for studying the pathogenesis of acute necrotizing pancreatitis by using bile acid. In acute necrotizing pancreatitis, the increased levels of lipid peroxidation products in tissues and the change in glutathione metabolism suggest ongoing peroxidation of lipids due to an enhanced generation of oxygen radicals. Therefore, antioxidant treatment can reduce tissue damage, biochemical alterations, and extrapancreatic complications, thus improving the final outcome.

Histopathologic Correlation of Magnetic Resonance Image Findings in Ischemic Necrosis of the Femoral Head (INFH) / 대한정형외과학회잡지

Magnetic resonance image of INFH were correlated with histologic sections. Seventeen patients withe eighteen hips were included in this study. reoperative radiographs and MRI were taken for the patients. Three hips were in stage II, nine hips were in stage III, and remaining six were in stage IV respectively(Ficat and Alert). These hips were replaced with artificial joint and resected heads were examined. The specimens were bisected along the imaging plane, and studied histologically and matched with respective MR images of T1 and T2. Specimen MRI was performed on three femoral head immediately after femoral head removal. Necrotic portion of the femoral head in earlier stage showed higher signal intensity in T1-weighted image. Subchondral void, necrotic bone and saponified fat were responsible for low signal intensity in necrotic portion. Low signal band adjacent to the necrotic foci represented inner fibrous tissue and outer reactive sclerotic bone. Outside the fibrous band, the signal intensity diminished compared with normal fatty marrow. these findings were attributed by cellular infiltration and trabecular bony proliferation. MRI patterns were variable in various stages, but corresponded well with histologic findings.