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通过向大鼠胰管注射玉米醇溶蛋白-油酸-亚油酸溶液诱导实验性慢性胰腺炎的病理生理学研究。

Pathophysiologic studies of experimental chronic pancreatitis in rats induced by injection of zein-oleic acid-linoleic acid solution into the pancreatic duct.

作者信息

Kataoka K, Sasaki T, Yorizumi H, Sakagami J, Kashima K

机构信息

Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kamigyoku, Japan.

出版信息

Pancreas. 1998 Apr;16(3):289-99. doi: 10.1097/00006676-199804000-00014.

DOI:10.1097/00006676-199804000-00014
PMID:9548669
Abstract

An experimental model of chronic pancreatitis was induced by a retrograde injection of a viscous solution consisting of zein-oleic acid-linoleic acid (0.05 ml/100 g body weight) into the rat pancreatic duct. Histologic and biochemical changes were investigated over a period of 6 months after induction of this model. The treated rats gained weight, but pancreatic weight decreased with time. Histologically, the widening of acinar lumen and cellular vacuolization occurred within 24 h at the parenchyma neighboring the small ducts filled with the injected solution. Degenerative parenchyma, interstitial edema, and inflammatory cell infiltration were pronounced 1 week later. Thereafter, duct-like tubular complex formation progressed, and the exocrine tissue exhibited marked atrophy of the gland with irregular fibrosis and fat replacement over a period of 6 months. Pancreatic contents of protein, amylase, DNA, and RNA markedly decreased, as did pancreatic weight, whereas hydroxyproline content increased. Oral administration of camostat did not affect pancreatic weight and contents of enzyme in this model. Urinary para-aminobenzoic acid (PABA) excretion in the BT-PABA test decreased to 54% at 6 weeks and 22% at 6 months. Although three quarters of pancreatic immunoreactive insulin (IRI) content was lost after 6 months, overt diabetes did not occur. The results suggest that an obstructive mechanism in the small ducts plays an important role in the genesis and development of chronic pancreatitis.

摘要

通过向大鼠胰管逆行注射由玉米醇溶蛋白 - 油酸 - 亚油酸组成的粘性溶液(0.05 ml/100 g体重)诱导建立慢性胰腺炎实验模型。在该模型建立后的6个月内对组织学和生化变化进行研究。治疗后的大鼠体重增加,但胰腺重量随时间下降。组织学上,在充满注射溶液的小导管附近的实质内,24小时内腺泡腔增宽和细胞空泡化就会出现。1周后,实质变性、间质水肿和炎性细胞浸润明显。此后,导管样管状复合体形成进展,在6个月的时间里,外分泌组织出现明显的腺体萎缩,伴有不规则纤维化和脂肪替代。胰腺中的蛋白质、淀粉酶、DNA和RNA含量显著下降,胰腺重量也下降,而羟脯氨酸含量增加。在该模型中,口服卡莫司他不影响胰腺重量和酶含量。BT - PABA试验中尿对氨基苯甲酸(PABA)排泄在6周时降至54%,在6个月时降至22%。尽管6个月后胰腺免疫反应性胰岛素(IRI)含量损失了四分之三,但未发生明显糖尿病。结果表明,小导管中的阻塞机制在慢性胰腺炎的发生和发展中起重要作用。

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