REGRESSION OF BILE-DUCT DAMAGE AND BILE-DUCT PROLIFERATION IN THE NON-REARTERIALIZED TRANSPLANTED RAT-LIVER IS ASSOCIATED WITH SPONTANEOUS GRAFT REARTERIALIZATION
Dl. Zhao et al., REGRESSION OF BILE-DUCT DAMAGE AND BILE-DUCT PROLIFERATION IN THE NON-REARTERIALIZED TRANSPLANTED RAT-LIVER IS ASSOCIATED WITH SPONTANEOUS GRAFT REARTERIALIZATION, Hepatology, 21(5), 1995, pp. 1353-1360
The aim of this study was to investigate the long-term consequences of
non-rearterialization of the graft in rat Liver transplantation. Live
r transplantation with (AOLT) and without graft rearterialization (NOL
T) was performed in anesthetized male Lewis rats. Quantitative morphom
etry and semiquantitative histopathology of the liver were performed a
t various times after operation. Volume fractions of tissue components
were determined, The number of arteries and bile ducts per portal tra
ct were measured in histological sections hom both groups. Hepatic blo
od flow was measured using the radioactive microsphere technique in ra
ts after NOLT (6 months). AOLT livers had a preserved lobular architec
ture at all time points and unaltered volume fractions. In addition, A
OLT livers maintained approximately one artery and one bile duct per p
ortal tract after transplantation. NOLT livers showed bile duct damage
at 3 days, cellular infiltration and ductular proliferation at 1 week
, increased ductular proliferation at 4 weeks, and fibrosis at 6 month
s. The volume fractions for nonhepatocyte parenchyma (3 days, 19.14 +/
- 1.29; week, 20.44 +/- 1.76; 4 weeks, 15.46 +/- 3.14), bile ducts/duc
tules (1 week 4.88 +/- 1.07; 4 weeks, 7.20 +/- 2.42); and connective t
issue (4 weeks, 4.02 +/- 1.66; 6 months, 14.94 +/- 0.63) were signific
antly increased. Hepatocyte volume fraction was signifcantly decreased
at all time points. A total of 1.58 +/- 0.08 arteries/portal tract we
re found in NOLT Livers after 4 weeks, rising to 2.44 +/- 0.10 arterie
s/portal tract after 6 months. At 6 months, hepatic arterial blood flo
w (0.69 mL/min/g) was significantly higher (P <.02) than control (0.25
mL/min/g). The findings indicate that NOLT leads to a time-dependent
overall derangement of liver structure, possibly due to bile duct dama
ge induced by lack of an arterial blood supply. Spontaneous graft rear
terialization may be responsible for the regression of bile duct damag
e and proliferation noted at the later stages. Nevertheless, biliary f
ibrosis may be a long-term consequence of NOLT.