LONG-TERM CONSEQUENCE OF RAT ORTHOTOPIC LIVER-TRANSPLANTATION WITH AND WITHOUT HEPATIC ARTERIAL RECONSTRUCTION - A CLINICAL, PATHOLOGICAL, AND HEMODYNAMIC-STUDY

Citation
H. Imamura et al., LONG-TERM CONSEQUENCE OF RAT ORTHOTOPIC LIVER-TRANSPLANTATION WITH AND WITHOUT HEPATIC ARTERIAL RECONSTRUCTION - A CLINICAL, PATHOLOGICAL, AND HEMODYNAMIC-STUDY, Hepatology, 26(1), 1997, pp. 198-205
Citations number
33
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
26
Issue
1
Year of publication
1997
Pages
198 - 205
Database
ISI
SICI code
0270-9139(1997)26:1<198:LCOROL>2.0.ZU;2-K
Abstract
Our aim was to investigate the time-related changes in various paramet ers following orthotopic rat liver transplantation with (AOLT) and wit hout (NOLT) arterial reconstruction in male Lewis rats. Body weight an d biochemical parameters were measured weekly, and a liver biopsy was obtained at 4, 8, and 12 weeks. Hemodynamics were evaluated at 12 week s using the microsphere technique and compared with matched controls. Following AOLT, rats gained weight normally without any noticeable com plication. In NOLT, two subgroups (NOLT-1 and NOLT-2) could clearly be identified retrospectively. In the NOLT-1 group, the body weight incr eased normally, although animals presented transient cholestasis. In t hese rats, the ductular proliferation found at 4 weeks had regressed b y the 12th week with near-normal biopsies. By contrast, in the NOLT-2 group, rats did not gain body weight and had persistent cholestasis. M arked ductular proliferation with increasing fibrosis was observed, re sulting in a secondary biliary cirrhosis by the 12th week. Surprisingl y, rearterialization of the grafted liver occurred in both NOLT-1 and NOLT-2 irrespective of their clinical course. All transplanted rats sh owed portal hypertension with marked portosystemic shunts, probably ca used by the portal cuff. However, a hyperdynamic circulatory state was only observed in the NOLT-2 group with cirrhotic changes. These findi ngs further show the combined role of an intact hepatic innervation an d of hepatocellular insufficiency in the genesis of the hyperdynamic c irculatory state associated with portal hypertension.