## Abstract Liver tumors, both primary and secondary, receive their main blood supply from the hepatic artery. Hepatic artery ligation (HAL) causes a reduction in tumor growth and tumor necrosis. In this experiment, three different experimental tumors were used to study the effect of hepatic artery
Influence of a reticuloendothelial-suppressing agent on liver tumor growth in the rat
✍ Scribed by Stefan Rydén; Lennart Bergqvist; Larsolof Hafström; Björn Hultberg; Unne Stenram; Sven-Erik Strand
- Publisher
- John Wiley and Sons
- Year
- 1984
- Tongue
- English
- Weight
- 656 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0022-4790
No coin nor oath required. For personal study only.
✦ Synopsis
Reticuloendothelial (RE) function was evaluated by measuring the biokinetics of a standardized 99Tcm-sulphur colloid. Methyl palmitate was administered intravenously on two consecutive days. A statistically significant reduction in the colloid uptake rate of the liver was registered after methyl palmitate administration. Histological examination revealed no signs of destruction of RE cells or microembolization. Inoculation of an experimental nitrosoguanidine-induced transplantable adenocarcinoma to the liver was performed in 16 rats one day after methyl palmitate administration and in 16 controls. Tumor size was significantly larger in methylpalmitate-treated animals at 7 and 14 days after inoculation. Survival was significantly decreased in methyl-palmitate-treated rats. These rats showed signs of fatty vacuolization and necrosis of liver parenchyma earlier than controls. Analyses of 0-hexosaminidase and lactate dehydrogenase revealed no deviation of enzyme levels either before or after tumor inoculation. The results indicate that a temporary suppression of RE function at the time of tumor inoculation may influence subsequent tumor growth.
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