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大鼠实验性胰腺炎。牛磺胆酸钠诱导的胰腺损伤的超微结构

Experimental pancreatitis in the rat. Ultrastructure of sodium taurocholate-induced pancreatic lesions.

作者信息

Aho H J, Nevalainen T J

出版信息

Scand J Gastroenterol. 1980;15(4):417-24. doi: 10.3109/00365528009181494.

Abstract

Necrotic lesions caused by the intraductal injection of sodium taurocholate in rat pancreas were studied by electron microscopy. The early (1 and 15 min after the injection) ductal cells were often necrotic. The acinar cell damage was characterized by mitochondrial swelling, vesiculation of the granular endoplasmic reticulum, and dissolution of cellular membranes. At later time intervals (1, 3, and 6 h) there were necrotic acinar cells with heterogeneous cytoplasmic inclusions representing degenerative cell organelles and their remnants. At 6, 12, and 24 h there were autophagic vacuoles in sublethally damaged acinar cells. The zymogen granules seemed relatively well preserved throughout the experiment. The vascular lesions consisted of endothelial detachment, extravasation of erythrocytes, thrombosis, and poikilocytosis. It was concluded that the initial cell injury was caused by the detergent action of the injected bile salt.

摘要

通过电子显微镜研究了大鼠胰腺中经导管注射牛磺胆酸钠引起的坏死性病变。早期(注射后1分钟和15分钟)导管细胞常发生坏死。腺泡细胞损伤的特征为线粒体肿胀、颗粒内质网囊泡化以及细胞膜溶解。在较晚的时间间隔(1、3和6小时),存在坏死的腺泡细胞,其细胞质内含物异质性,代表退化的细胞器及其残余物。在6、12和24小时,亚致死损伤的腺泡细胞中出现自噬空泡。在整个实验过程中,酶原颗粒似乎保存相对良好。血管病变包括内皮细胞脱离、红细胞外渗、血栓形成和异形红细胞症。得出的结论是,最初的细胞损伤是由注射的胆盐的去污剂作用引起的。

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