Takada T, Yasuda H, Uchiyama K, Hasegawa H, Shikata J, Takada K
First Department of Surgery, Teikyo University School of Medicine, Tokyo, Japan.
Gastroenterol Jpn. 1989 Feb;24(1):54-9. doi: 10.1007/BF02774871.
The factors inducing biliary dilatation were studied morphologically and functionally by cholangiography and cholangiomanometry in experimental models of chronic biliary dilatation. These models were produced by four methods: Constriction of the lower bile duct (Group 1), formalin infusion into the duodenal papilla (Group 2), detachment of the extrahepatic bile duct (Group 3), and sphincterotomy (Group 4). Biliary dilatation was observed in the first three groups but not in the fourth group. An increase in the intraductal pressure due to blockage of the biliary outflow tract was considered to be the cause of biliary dilatation in Group 1 and 2. In Group 3, the function of the lower bile duct, including the papilla was intact, and reduced resistance of the bile duct wall and due to the loss of the support from the surrounding connective tissue was considered to have induced biliary dilatation. These results suggest that experimental chronic biliary dilatation can be produced by two approaches: 1) Blockage of bile flow in the papilla or the bile duct, and 2) detachment of the bile duct without disturbing bile flow.
通过胆管造影和胆管测压，在慢性胆管扩张的实验模型中对引起胆管扩张的因素进行了形态学和功能学研究。这些模型通过四种方法构建：胆管下端缩窄（第1组）、向十二指肠乳头注入福尔马林（第2组）、肝外胆管游离（第3组）和括约肌切开术（第4组）。前三组观察到胆管扩张，而第四组未观察到。由于胆管流出道阻塞导致的导管内压力升高被认为是第1组和第2组胆管扩张的原因。在第3组中，包括乳头在内的胆管下端功能完好，胆管壁阻力降低以及由于周围结缔组织支撑丧失被认为诱发了胆管扩张。这些结果表明，实验性慢性胆管扩张可通过两种方法产生：1）乳头或胆管胆汁流动受阻，以及2）胆管游离而不干扰胆汁流动。
