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Influence of portal branch ligation on the outcome of repeat dearterializations of an experimental liver tumor in the rat
Author(s) -
Wang LiQing,
Persson Bo G.,
Stenram Unne,
Bengmark Stig
Publication year - 1994
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930550406
Subject(s) - ligation , medicine , liver lobe , portal vein , necrosis , liver tumor , pathology , gastroenterology , nuclear medicine , hepatocellular carcinoma
It has been suggested that the portal vein should be occluded during intermittent hepatic dearterialization in order to induce a more complete ischemia of the tumor. In this experiment the influence of portal branch ligation in combination with repeat dearterializations on a liver tumor was investigated. Twenty‐seven rats were randomly allocated to sham treatment (n = 6); portal branch ligation (PBL) (n = 7); 120 min of repeat dearterialization (n = 7); and portal branch ligation (PBL) in combination with 50 min of repeat dearterialization (n = 7) (once a day during 5 days). The results showed that portal branch ligation alone did not alter the tumor growth compared with sham treatment ( P > 0.05), nor did portal branch ligation in combination with repeat dearterializations for 50 min ( P > 0.05). However, tumor growth delay was achieved following 120 min of repeat dearterializations without occlusion of the portal branch ( P < 0.01 versus all the other groups). There was a significant weight loss of the lobe undergoing PBL, whether dearterialization was added or not ( P < 0.001). The liver nucleotide/DNA and RNA/DNA ratio significantly decreased as well. Histological examination showed that > 50% of tumor cells became necrotic after repeat dearterializations for 2 hr indicating a significant damage to tumor tissue. In contrast, PBL in combination with repeat dearterializations for 50 min induced extensive liver necrosis without having any influence on tumor growth. © Wiley‐Liss, Inc.