Metastasis and the reticuloendothelial system. II. Effect of triamcinolone acetonide on organ retention of malignant cells in endotoxin-treated mice.
The lung retention patterns of B16 melanoma cells were determined after intravenous injection of [125i]dUrd-labelled tumor cells into B16 melanoma-bearing mice. Experiments were performed to assess the effects of a synthetic glucocorticoid, triamcinolone acetonide, on the retention of B16 melanoma cell arrested in the lungs of mice with endotoxin-induced reticuloendothelial system hyperfunction. Lung clearance of malignant cells was greatly accelerated in mice treated with endotoxin alone but was markedly inhibited in mice with only triamcinolone acetonide. In mice treated with both endotoxin and subsequently triamcinolone acetonide after tumor-cell arrest processes had occurred, the endotoxin-induced increase in clearance was nullified. These results are discussed in terms of the mutually antagonistic activity of both pharmacologic agents upon the reticuloendothelial system and the role of the latter in regulating organ retention of disseminated malignant cells.
D000818:Animals; D004731:Endotoxins / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects; D008175:Lung Neoplasms / Q000473:pathology / Q000556:secondary*; D008297:Male; D008545:Melanoma / Q000473:pathology / Q000556:secondary; D051379:Mice; D008810:Mice, Inbred C57BL; D012157:Mononuclear Phagocyte System / Q000187:drug effects*; D009362:Neoplasm Metastasis / Q000503:physiopathology*; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000473:pathology / Q000556:secondary; D009360:Neoplastic Cells, Circulating; D014222:Triamcinolone Acetonide / Q000494:pharmacology*
D004731:Endotoxins; D014222:Triamcinolone Acetonide