Xia Y F
Department of Pathology, Wuhan General Hospital, Guangzhou Unit PLA.
Zhonghua Bing Li Xue Za Zhi. 1993 Feb;22(1):30-2.
Electron microscopical and immunoelectron microscopical techniques were employed to investigate the pathogenesis of sodium taurocholateinduced acute pancreatitis. It was demonstrated that the necrosis of pancreatic acinar cells was associated with specific intracellular vacuolation. A continuous course of vacuole formation from zymogen granules was observed. There were of ten several vacuoles inside one acinar cell, and most of the vacuoles were distributed among zymogen granules. These vacuoles contained large amounts of filamentous materials, which were proved to be pancreatic digestive enzymes by immunoelectron microscopical labelling for alpha-amylase and able to digest and disrupt the circumferential organelles. The results of this study suggest that the necrosis of acinar cells was caused by the activation of digestive zymogen inside zymogen granules. As trypsin is the only enzyme which could activate all the digestive zymogen, and trypsinogen is the sole zymogen capable of autoactivation, it is suggested that the autoactivation of trypsinogen plays an important role in the pathogenesis of acute pancreatitis.
采用电子显微镜和免疫电子显微镜技术研究牛磺胆酸钠诱导的急性胰腺炎的发病机制。结果表明,胰腺腺泡细胞的坏死与特定的细胞内空泡形成有关。观察到从酶原颗粒开始的连续空泡形成过程。一个腺泡细胞内常常有几个空泡,且大多数空泡分布在酶原颗粒之间。这些空泡含有大量丝状物质,通过对α-淀粉酶进行免疫电子显微镜标记证明这些丝状物质是胰腺消化酶,并且能够消化和破坏周围的细胞器。本研究结果表明,腺泡细胞的坏死是由酶原颗粒内消化酶原的激活引起的。由于胰蛋白酶是唯一能够激活所有消化酶原的酶,且胰蛋白酶原是唯一能够自动激活的酶原,因此提示胰蛋白酶原的自动激活在急性胰腺炎的发病机制中起重要作用。