REGRESSION OF BILE-DUCT DAMAGE AND BILE-DUCT PROLIFERATION IN THE NON-REARTERIALIZED TRANSPLANTED RAT-LIVER IS ASSOCIATED WITH SPONTANEOUS GRAFT REARTERIALIZATION

Citation
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
Citations number
32
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
21
Issue
5
Year of publication
1995
Pages
1353 - 1360
Database
ISI
SICI code
0270-9139(1995)21:5<1353:ROBDAB>2.0.ZU;2-E
Abstract
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.