Kagaya T, Takebe T, Koizumi M, Kataoka S, Kamei T, Oyama K
Gastroenterol Jpn. 1979 Aug;14(4):327-35. doi: 10.1007/BF02774229.
To elucidate the pathophysiological process of alcoholic pancreatitis, chronic alcohol intoxication was made in Wistar rats on balanced diet giving 20% ethanol freely for 60 weeks. The control rats received water. Histological picture of the pancreas, hormonal activity in the mucosa of upper digestive tract and the nature of pancreatic juice were examined in every 15th week. The results were as follows. 1) No histological changes were noted in the pancreas of control group. In the ethanol group, morphological abnormalities of the pancreas appeared after 30 weeks. Of the histological findings, the changes on the ductal system such as dilatation of pancreatic duct, plug formation in the ductal lumen and periductal fibrosis were significant. 2) The long term ethanol administration tended to decrease the amounts of gastrin, secretin and cholecystokinin contained in the gastrointestinal mucosa. 3) Regardless of the histological changes of the pancreas, almost no changes were noted in the bicarbonate and protein concentration during the experimental period of 60 weeks. From the above results, a mechanism obstructing pancreatic ductal system is considered to be important in the pancreatic lesions by alcohol rather than a mechanism of stimulating pancreatic exocrine secretion.
为阐明酒精性胰腺炎的病理生理过程,对喂食均衡饮食的Wistar大鼠进行慢性酒精中毒造模,自由饮用20%乙醇,持续60周。对照组大鼠饮用清水。每隔15周检查胰腺的组织学图像、上消化道黏膜的激素活性以及胰液的性质。结果如下:1)对照组大鼠胰腺未发现组织学改变。乙醇组大鼠在30周后出现胰腺形态学异常。在组织学检查结果中,导管系统的改变,如胰管扩张、管腔内堵塞物形成和导管周围纤维化较为明显。2)长期给予乙醇往往会使胃肠道黏膜中胃泌素、促胰液素和胆囊收缩素的含量降低。3)在60周的实验期内,无论胰腺的组织学改变如何,碳酸氢盐和蛋白质浓度几乎没有变化。根据上述结果,酒精导致胰腺病变的重要机制被认为是阻塞胰管系统,而非刺激胰腺外分泌的机制。