HETEROTOPIC LIVER-TRANSPLANTATION IN RATS - EFFECT OF INTRAHEPATIC ISLET ISOGRAFTS AND SPLIT PORTAL BLOOD-FLOW ON LIVER INTEGRITY AFTER AUXILIARY LIVER ISOTRANSPLANTATION

Background. Auxiliary heterotopic liver grafts atrophy in the absence of portal venous inflow; evidence suggests that an islet-derived hepat otrophic factor may exist in the portal drainage. Here we examine the effects of intrahepatic islet isografts in maintaining hepatocyte inte grity in Wistar Furth rats with one of several types of arterialized a uxiliary liver isografts. Methods. In type 1 procedures the auxiliary liver was interposed into the recipient infrarenal vena cava and perfu sed through the graft portal vein with caval blood. In type 2 procedur es the donor infrahepatic vena cava was anastomosed end-to-side to the recipient vena cava and the recipient portal vein was diverted to the graft portal vein. Both types of auxiliary grafts were arterialized; bile duct drainage was through the duodenum. Syngeneic islets were iso lated and embolized into the portal veins of one half of the donor typ e I or native type 2 livers (1500 to 1700 islets). Finally, we perform ed six type 3 procedures in which a type 2 procedure was performed exc ept that the portal blood flow was split so that the portal vein recei ving the splenic, gastric, pancreatic, and duodenal drainage supplied the native liver and that the common mesenteric vein supplied the auxi liary graft with equivalent portal blood flow. Atrophy in heterotopic and native livers were compared for the three models after 3 months. R esults. Intrahepatic islets in type 1 auxiliary liver isografts withou t portal venous inflow did not prevent graft atrophy. Conversely, nati ve livers deprived of portal venous inflow in our type 2 procedures, r egardless of the presence of intrahepatic islet isografts, atrophied r elative to auxiliary liver grafts in which portal venous inflow was pr ovided by diverting the recipient's portal vein to the graft. In type 3 recipients atrophy was greater in the native livers than in the graf ts. Conclusions. The results of our study suggest that islet-derived f actors are not sufficient to prevent hepatocellular atrophy in auxilia ry rat liver transplantation models and that a potent hepatotrophic fa ctor may exist in the venous drainage of the bowel distal to the duode um.