Acute and extensive hepatic cell necrosis was produced experimentally in rabbits by means of the Shwartzman mechanism using adeno- and hepatitis B viruses. The change that occurred in the liver was quite severe, namely, areas of hemorrhagic necrosis of various sizes in gross appearance and lytic-coagulative necrosis with hemorrhage and leukocyte-mononuclear cell infiltration histologically. Thrombi formation was noted in and around the necrotic areas, and it was not unusual to see necrosis of an entire lobe. This seems to be a model, to some extent, for human fulminant hepatitis caused by hepatitis virus infection, and suggested that some nonspecific reaction such as intravascular clotting may also play an important role in causing or complicating acute, severe, and extensive necrosis of the liver in human cases. Heparin administration very effectively prevented such hepatic necrosis, which supports the view that the change we observed in the liver was really the Schwartzman reaction; further, it is reminiscent of the fact that heparin administration is sometimes effective in fulminant hepatitis treatment if given at te appropriate stage of the disease.