Characterization of tumor-induced inflammation and the effect of some anti-inflammatory drugs on the increased vascular permeability.
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 (GSH). 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. The action of glucocorticoids on the tumor-induced vascular hyper-permeability was discussed in connection with a tumor factor possibly responsible for the vasoexudation.
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002199:Capillary Permeability / Q000187:drug effects*; D002286:Carcinoma, Ehrlich Tumor / Q000098:blood supply / Q000150:complications* / Q000503:physiopathology; D005070:Evans Blue; D005119:Extravasation of Diagnostic and Therapeutic Materials; D005978:Glutathione / Q000494:pharmacology; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008813:Mice, Inbred ICR; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D012867:Skin / Q000098:blood supply; D013950:Thymus Gland / Q000503:physiopathology; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D005070:Evans Blue; D005978:Glutathione