When rats received
endotoxin 48 hours after two-thirds liver resection, 50% of them died within 12 hours with
massive hepatic necrosis at a dose that did not affect
sham-operated rats. In the hepatic sinusoids,
fibrin deposition and endothelial cell destruction occurred 5 hours after
endotoxin administration. When
antithrombin III concentrate was infused concomitantly with
endotoxin administration, all rats survived 12 hours, and the extent of hepatic
necrosis and the deranged serum
glutamic pyruvic transaminase values were significantly attenuated at 5 hours compared with those in the control rats. Similar improvements in the incidence of mortality and liver injury were observed
after treatment with
gum arabic before
hepatectomy. The stimulatory state of Kupffer cells based on the ability to produce
superoxide anions estimated by
formazan deposition after liver perfusion with nitro blue tetrazolium and
phorbol myristate acetate was increased between 24 and 72 hours after operation. This increase disappeared after
gum arabic treatment. It is concluded that
massive hepatic necrosis can occur as a result of sinusoidal
fibrin deposition provoked by
endotoxin in partially hepatectomized rats. Activated Kupffer cells may contribute to this provocation.