| PART I Pathology of Local Lesions in the Acute Phase of Acute PancreatitisIn this study, a rat model of acute biliary pancreatitis established by retrograde injection of sodium taurocholate into the pancreatocholangitic duct was adopted for experiment. Under comparable conditions of model preparing, characteristics of primary (pancreatic edema, pancreatic hemorrhage or necrosis) and secondary lesions (peripancreatic edema, hemorrhagie, necrosis and ascites) were observed and their interrelationship was explored combined with pathologic findings. I .Gross pathologic findings1. In the edematous group, pancreatic tissues ranged from mild to highly edematous with possibly tense envelopes; lobular septa were clear. Ascites formation could be seen in a part of the rats. In the necrotizing group, apart form the above manifestations, there were hemorrhage and necrosis in the pancreas, with comparatively large amounts of ascites in most of the rats. In the control group, except for yellowish ascites formation in several rats, no significant pancreatic edema andenvelope tension were observed.2. At the same interval after model establishment, except for the edema scores in the necrotizing group and edematous group as well as the necrosis scores in the edematous group and control group, other differences among the groups were very significant(P<0.01). At different intervals (3h and 6h), no significant differences existed in the same model(P>0.05), except in the edematous group, pancreatic fat necrosis scores were significantly different(P<0.05).3. A positive correlation existed between primary (pancreatic edema and hemorrhage and necrosis) and secondary lesions (peripancreatic edema and hemorrhagic necrosis). Pancreatic hemorrhage was more significant than pancreatic edema(P<0.01).II .Microscopic pathologic findings1. In the control group, except for mild edema, the pancreatic structures were completely normal. In the edema group, the main manifestation was interstitial edema of various degrees. Infiltration of neutrophils and focal necrosis could be observed. In the necrotizing group, apart from the above findings, interstitial hemorrhage and necrosis of small vessels could be seen. Neutrophil infiltration with various degrees could be found in the interstitial, among alveoli and around blood vessels. Acinar cells displayed necrosis of various degrees and obscure structures.2. At the same interval, there were no significant differences of pancreatic necrosis and peripancreatic infiltration between the necrotizing group and the edematous one. Other lesions were significantly different. (P<0.05). At different intervals, no significant microscopic differences were found in the same group.III. Exceptional pathologic findings1. Mild pancreatic edema or necrosis with extensive infiltration in the retroperitoneal space: In one case, pancreatic edema and hemorrhagic necrosis were restricted in the pancreatic head, but were complicated with extensive retroperitoneal infiltration and blood ascites. Microscopic findings were definite edema of pancreatic interstitial and widened interstitial spaces.2. Severe pancreatitc edema or hemorrhagic necrosis with localized retroperitoneal infiltration: 3 cases presented with comprehensive pancreatic edema and hemorrhagic necrosis, but peripancreatic infiltration was restricted to left perirenal space in 2 cases and right perirenal space in 1 case. Two rats presented with severe comprehensive pancreatic edema but without retroperitoneal infiltration, of which, one had no ascites, one had 1.5ml yellowish ascites.3. Hemorrhagic necrotizing model with severe lesions of spleen hilum: Five cases developed spleen infarct, one involving the whole spleen, 2,the central areas and one, the upper pole and another, the lower pole.4. Under comparable conditions of model preparation, the discrepancy oflocal lesions may be related to differences of local tissue structures. IV. The pancreatic interstitial, envelop a...
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