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大鼠蛙皮素和牛磺胆酸盐急性胰腺炎时的肝脏超微结构

The liver ultrastructure in caerulein and taurocholate acute pancreatitis in the rats.

作者信息

Andrzejewska A, Długosz J W, Jurkowska G

机构信息

Department of Pathological Anatomy, Medical Academy of Białystok.

出版信息

Rocz Akad Med Bialymst. 1998;43:117-36.

PMID:9972048
Abstract

The purpose of the study was to compare the morphological alterations of the liver in two models of acute pancreatitis: caerulein-induced (edematous) and taurocholate-induced (necro haemorrhagic one). The experiments were performed on 24 male, Wistar rats, weighing 240-260 g. In group I (n = 8) the supramaximal stimulation with i.v. caerulein (5 micrograms/kg/h) during 12 h was applied (C-AP). Control animals (group II, n = 4) received i.v. saline (C-C). In group III (n = 8) 5% sodium taurocholate (0.2 ml/min) was injected into the bile-pancreatic duct during sterile laparotomy (T-AP). In group IV (n = 4) animals were sham operated (T-C). The specimens of the liver were excised after decapitation of rats at 12 h after beginning of caerulein infusion or intraductal injection of sodium taurocholate. The light and electron microscopy was performed. The marked hepatic lesion were found in both variants of experimental pancreatitis, however they were far more advanced in taurocholate pancreatitis. In light microscopy the dispersed foci of colliquative necrosis, degeneration of hepatocytes, swelling of Kupffer cells predominated in taurocholate pancreatitis. The glycogen deposits were depleted but lipid droplets were increased in size and number. The swelling of mitochondria, degeneration of their matrix and cristae, increase of autophagocytosis and numerous lysosomes, the lesions of sinusoids with increased activity of phagocytic cells were more evident in taurocholate pancreatitis--(more severe model of the disease). These findings document severe injury to the liver in acute pancreatitis depending on the severity of inflammatory process in pancreas. They also suggest that the liver could be not only passive target of pancreatogenic noxa in acute pancreatitis, but it could be also a defensive barrier against spreading of injuring agents on other system. This role seems to be especially evident in more severe form--taurocholate induced pancreatitis.

摘要

本研究的目的是比较两种急性胰腺炎模型中肝脏的形态学改变

蛙皮素诱导的(水肿型)和牛磺胆酸钠诱导的(坏死出血型)。实验选用24只体重240 - 260 g的雄性Wistar大鼠进行。在第一组(n = 8)中,通过静脉注射蛙皮素(5微克/千克/小时)进行12小时的超最大刺激(C - AP)。对照组动物(第二组,n = 4)静脉注射生理盐水(C - C)。在第三组(n = 8)中,在无菌剖腹手术期间向胆胰管注射5%牛磺胆酸钠(0.2毫升/分钟)(T - AP)。在第四组(n = 4)中,动物进行假手术(T - C)。在蛙皮素输注或胆管内注射牛磺胆酸钠开始后12小时,将大鼠断头后取出肝脏标本。进行光镜和电镜检查。在两种实验性胰腺炎模型中均发现明显的肝脏病变,然而在牛磺胆酸钠诱导的胰腺炎中病变更为严重。在光镜下,牛磺胆酸钠诱导型胰腺炎中以散在的液化性坏死灶、肝细胞变性、库普弗细胞肿胀为主。糖原沉积减少,但脂滴的大小和数量增加。线粒体肿胀、其基质和嵴变性、自噬增加以及大量溶酶体,吞噬细胞活性增加的窦状隙病变在牛磺胆酸钠诱导型胰腺炎中更为明显——(该疾病更严重的模型)。这些发现证明了急性胰腺炎时肝脏损伤的严重程度取决于胰腺炎症过程的严重程度。它们还表明,肝脏在急性胰腺炎中不仅可能是胰腺毒性物质的被动靶器官,而且还可能是防止损伤因子扩散到其他系统的防御屏障。这种作用在更严重的形式——牛磺胆酸钠诱导的胰腺炎中似乎尤为明显。

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