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作 者:吕维富[1] 季学兵[1] 张行明[1] 杨秋红[1] 叶兴梅[1] 许实成[1] 张学彬[1]
出 处:《医学影像学杂志》2001年第1期16-18,共3页Journal of Medical Imaging
摘 要:目的 :探讨胰腺分裂 (PD)在慢性胰腺炎病因学中的作用及其发病机制。方法 :将 32只犬随机分为 4组 (每组8只 )。Ⅰ组 :部分结扎背 -腹胰管间的交通支。Ⅱa组 :切断并结扎交通支。Ⅱb组 :在背胰管注入小乳头前 2mm处将其切断并结扎断端。Ⅲ组 :假手术对照组 ,除不结扎交通支外 ,其余操作同上。于手术前检测各组犬的血清磷脂酶(PLA2 )和淀粉酶 (Ams)活性及背、腹胰管基础压并在胰泌素激发后 15、30、45、6 0和 90分钟各测压一次。于术后 180天再行胰胆管测压和造影并观察背、腹胰和十二指肠乳头的病理改变。结果 :(1)Ⅰ、Ⅱa组和Ⅱb组术后 5~ 80天血清PLA2 和Ams活性显著升高。 (2 )处死时Ⅰ、Ⅱa组腹胰管和Ⅱb组背、腹胰管压力在激发后 30~ 6 0分钟显著高于注药前(P <0 .0 1) ;在 6 0分钟后 ,前两组压力恢复到术前水平 (P >0 .0 5 ) ,而Ⅱb组仍较高 (P <0 .0 5 ) ,该组压力在 90分钟后恢复正常。 (3)光镜 :Ⅱb组犬背、腹胰小叶间或 /和胰管周围显著纤维组织增生 ,腺细胞结构破坏和炎细胞浸润。Ⅰ和Ⅱa组腹胰见轻度上述改变。 (4 )电镜 :Ⅰ、Ⅱa组腹胰和Ⅱb组背、腹胰腺细胞粗内质网脱颗粒、融合和扩张。酶原颗粒减少 ,线粒体肿张。Ⅰ和Ⅱa组背胰及Ⅲ组背、腹胰未见异常。结论 :PD是慢性胰腺炎的病因学?Objective:To clarify the etiologic association of pancreas divisum(PD)with chronic pancreatitis and the pathogenesis.Methods:A canine model of PD was established in 32 dogs.The dogs were randomly divided into 4 groups(each n=8).Group Ⅰ:The communicating branch between the dorsal and ventral pancreatic duct was partly ligated remaining a 1.0 mm diameter.Group Ⅱa:The communicating branch was amputated and ligated.Group Ⅱb:The dorsal duct was amputated and ligated at 2 mm distance to the minor papilla.Group Ⅲ:A sham operation without any amputation or ligation was performed.Before and after operation,the activities of serum phospholipases A 2(PLA 2)and amylase (Ams)were assayed and the basal pressures of the ducts were measured when secretin was injected.Pancreatic ductography and the pathologic examination were performed.Results:(1)The activities of serum PLA 2 and Ams in Group Ⅰ,Ⅱa and Ⅱb were significantly increased 5~80 days after operation.(2)At sacrifice,the basal pressures of the ventral duct were significantly increased 30~60 min after provocation in Group Ⅰ,Ⅱa and Ⅱb,especially in Group Ⅱb,the pressures returned to the normal level till 90 min.The pressures of the dorsal duct were significantly increased in Group Ⅱb but no difference in Group Ⅰ and Ⅱa.(3)Light microscope:The fibrosis of inter-lobus and periducts,the destruction of acini and infiltration of inflammatory cell in dorsal and ventral pancreas were found in Group Ⅱb.But in Group Ⅰand Ⅱa,this findings were present only in the ventral pancreas.(4)Electron microscope:In ventral pancreas of Group Ⅰand Ⅱa and the dorsal and ventral pancreas of Group Ⅱb,the rough endoplasmic reticulum of the acinar cells showed granules-scaling,fusion and dilatation.The zymogen granules decreased and the mitochondria was swollen.Conclusion:A difinite etiologic relationship was confirmed between PD and chronic pancreatitis.The pathogenesis was due to the functional obstruction of the minor papilla at the peak stage of se
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