To verify whether endotoxin (LPS) might act as a priming cofactor of liver
injury caused by obstructing the duodenum, four groups of male Wistar rats
were studied. The first two groups comprised rats in which a closed duodena
l loop (CDL) was created: CDL, n = 6 and CDL + LPS, n = 7; the next two gro
ups comprised sham-operated animals: Sham n = 6 and Sham + LPS, n = 6. LPS,
400 mu g/kg bodyweight, was administered i.p, to the rats belonging to gro
ups CDL + LPS and Sham + LPS, 24 h before laparotomy. Twenty-four hours aft
er laparotomy the animals were killed. Damage to bile ducts, extent and gra
ding of coagulative and lytic spotty necrosis in liver tissue were evaluate
d morphologically. Coagulative necrosis was severe in four of seven rats of
the group CDL + LPS, mild in six of six rats of group CDL, and absent in f
our of six and five of six rats of groups Sham and Sham + LPS (chi(2) 32.8,
P = 0.0001). The animals of group CDL + LPS had more frequently diffuse ly
tic spotty necrosis than the animals in the three other groups (chi(2) 9.57
P < 0.01). The results of our study indicate that, in rodents subjected to
a closed duodenal loop, priming with LPS exacerbates liver injury due to c
holate stasis.