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Induce Ascitic Fluid in Mice1
Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College, Kawada-cho 8-1 Shinjuku-ku [E. O., T. Y., Y. K., N. O., H. D.], and Research Institute for Growth Science Wakamatsu-cho Shinjuku-ku, [M. O., K. S.], Tokyo 162, Japan
Recent studies have suggested that pleural or peritoneal effusion associated with metastatic tumors is induced by some mediators produced by the tumor cells. We studied the ability of well-characterized peptide growth factors to produce ascites in mice. Peritoneal administration of epidermal growth factor (EGF, 10 to 40 µg/mouse/wk) or transforming growth factor
(TGF-
, 10 to 40 µg/mouse/wk) via osmotic minipumps resulted in formation of bloody ascites. The amount of ascites produced was dependent on the dose of growth factors. Vehicle alone or insulin-like growth factor I (40 µg/mouse/wk) was without effect. Indomethacin, a blocker of prostaglandin synthesis, significantly reduced the ascites accumulation induced by EGF, suggesting that prostaglandins are involved in ascites formation induced by EGF. Dexamethasone was also effective in attenuating the effect of EGF. Thus, it is possible that peritoneal effusion associated with disseminated tumors is, at least in part, due to EGF-like materials (most likely TGF-
) produced by tumor cells. The mechanism by which these peptides induce bloody ascites is not known for certain, but it may be due to the reported activity for neovascularization or increased vascular permeability.
1 This work was supported by grants from the Ministry of Education, the Ministry of Health and Welfare, and the Foundation for Growth Science.
2 To whom requests for reprints should be addressed.
Received 12/ 4/89.
Revised 4/23/90.
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