@article{oai:niigata-u.repo.nii.ac.jp:00023341,
 author = {佐藤, 徳光 and 新村, 末雄 and 藤巻, 雅邦 and 藤沢, 信義 and 前田, 宜俊},
 issue = {9},
 journal = {新潟医学会雑誌, 新潟医学会雑誌},
 month = {Sep},
 note = {The vascular bed in a murine dermal tissue responded to inoculated tumor cells by two-phased changes in the vascular permeability. The initial increase in the vascular permeability was seen in an early stage (1 to 3 day post tumor cells inoculation), and the inflammation was sensitive to glutathione. Glucocorticoids reduced the increased vascular permeability, but neither acetylsalicylic acid nor indomethacin did. The later vascular response was produced by a growing solid tumor in a continuous mode beginning at 5th to 10th day post inoculation. The degree of the increased vascular permeability in this chronic phase was in direct proportion to the wet weight of the solid tumor, and the inflammation was insensitive to glutathione. Glucocorticoids reduced the increased vascular permeability, but neither acetylsalicylic acid nor indomethacin did. Increased vascular permeability was inducible by the subcutaneous injection of a solid tumor extract rich in γ-globulins precipitable at　20-33%　saturation of ammonium sulfate. The vascular permeability-increasing activity of the tumor extract was reducible in the presence of highly polymerized dextran sulfate (DS-500) which showed a strong anticomplementary activity, but not by other substances such as dextran sulfate with a low molecular weight, nonsulfated dextran, chondroitin sulfate or heparin. As the tumor extract includes γ-globulins in aggregated or bound form and adsorbs complements, it is assumed that the aggregated γ-globulins increase vascular permeability by triggering the complement activation system in the skin. DS-500 might antagonize the process.},
 pages = {546--558},
 title = {癌により誘発される血管透過性亢進像},
 volume = {102},
 year = {1988}
}