Svanvik J, Thornell E, Zettergren L
Surgery. 1981 Apr;89(4):500-6.
Experimental cholecystitis was induced by implanting gallstones from human beings into the gallbladder of the cat. Three months later the concentrating function of the gallbladder, the motility, and hepatic bile flow were studied by a perfusion technique in the anesthetized animal. Gallbladder function was correlated to morphologic changes. After 3 months, the cystic duct was patent in nine animals and bile was found in the gallbladder. In 17 animals the cystic duct was obstructed and colorless contents were found in the gallbladder. Animals with a patent cystic duct showed slight or moderate inflammation and intact concentrating activity in the gallbladder, whereas animals with obstructed animals had pronounced inflammation and continuous fluid "secretion" into the lumen. Both groups had increased bile outflow from the liver. Indomethacin, a prostaglandin synthetase inhibitor, promptly reversed gallbladder fluid "secretion" into absorption and reduced the increased bile flow to a normal level. These results are discussed in relation to clinical findings in man. A mechanism by which prostaglandins are responsible for the inflammatory gallbladder "secretion" and the increased bile flow from the liver is proposed.
通过将人类胆结石植入猫的胆囊来诱发实验性胆囊炎。三个月后,在麻醉动物身上采用灌注技术研究胆囊的浓缩功能、运动性和肝胆汁流量。胆囊功能与形态学变化相关。三个月后,9只动物的胆囊管通畅,胆囊内有胆汁。17只动物的胆囊管阻塞,胆囊内发现无色内容物。胆囊管通畅的动物胆囊有轻微或中度炎症且浓缩活性完好,而胆囊管阻塞的动物有明显炎症且持续有液体“分泌”到腔内。两组动物肝脏的胆汁流出均增加。前列腺素合成酶抑制剂吲哚美辛能迅速使胆囊液体“分泌”转变为吸收,并使增加的胆汁流量降至正常水平。结合人类的临床发现对这些结果进行了讨论。提出了一种前列腺素导致炎症性胆囊“分泌”和肝脏胆汁流量增加的机制。