STUDIES INTO THE MECHANISM OF REVERSAL OF EXPERIMENTAL ACUTE HEPATIC-FAILURE BY HEPATOCYTE TRANSPLANTATION .1.

  • 1 January 1981
    • journal article
    • research article
    • Vol. 24  (1) , 39-44
Abstract
Single cell suspensions of syngeneic, allogeneic and xenogeneic hepatocytes apparently can significantly improve survival in a rat model of acute hepatic failure induced by D-galactosamine. The mechanism by which hepatocyte transplantation reverses the toxin-induced hepatic necrosis is explored. Radioautographic studies indicated that i.p. administered hepatocytes labeled with tritiated thymidine did not repopulate the injured recipient liver. Hepatocytes irradiated with 10,000 rad (i.e., the cells were nonreplicating) also resulted in a significant (P < 0.001) increase in animal survival when given to rats treated with D-galactosamine. Experiments with subcellular fractions of hepatocytes demonstrated that an intact cell was not required and that a heat stable factor (or factors) present in the cytosol fraction, which is not insulin or glucagon, is responsible for the increase in survival observed. This factor appears to increase the rate of endogenous regeneration of the injured recipient liver.