Hepatic arterial interruption in the fetus—An attempt to simulate biliary atresia

Abstract

Investigation of biliary atresia is hampered by the lack of suitable experimental models. The development of a technic of producing biliary atresia artificially would be extremely useful. Extrahepatic biliary atresia can be simulated by ligation of the common bile duct; intrahepatic atresia by selective destruction of the intrahepatic bile ducts. Since the work of Cameron and Mayes, 1 it has been appreciated that the intrahepatic biliary tree and the hepatic parenchyma enjoy different blood supplies, 2 ligation of the hepatic artery should produce selective ischemia of the intrahepatic bile ducts. Such ligation in the postnatal animal has often resulted in necrosis of both hepatic parenchyma and biliary ducts. 3–5 However, the fetal mammal, with highly oxygenated umbilical venous blood in communication with the portal veins, might suffer ischemia of the biliary tree without parenchymal necrosis. Ischemia of a fetal tissue frequently results in atrophy of that tissue without inflammaton; 6,7 therefore, ischemia of the fetal biliary tree might lead to disappearance of the intrahepatic ducts without infarct. This paper reports an effort to test these hypotheses in the fetal rabbit. The rabbit was selected because of efficiency of breeding, with the realization that the anatomy of the hepatic artery and its collateral circulation is variable in the rabbit, that rabbits have poor maternal instincts, and that this animal is susceptible to coccidiosis, a necrotizing disease of bile ducts and liver. Despite these handicaps, the experiments have yielded encouraging results which warrant report.