The effects of oxygen radicals on pulmonary edema formation.
This article is a review of the current literature concerning the possible involvement of oxygen radicals in the development of pulmonary edema. The article focuses on changes in capillary endothelium caused by many different imposed experimental conditions that may be related to the generation of O2, OH. or H2O2. Data from our laboratory show that scavengers such as superoxide dismutase, dimethylsulfoxide, and catalase as well as leukocyte depletion provide partial protection to the very caustic alpha-naphthylthiourea. The literature concerning the possible involvement of leukocyte or tissue generation of oxygen radicals in the various forms of pulmonary edema is combined into a simple model that may explain why pathologic tissues show variable responses to compounds that should either scavenge the oxygen radicals or prevent leukocyte involvement.
D002199:Capillary Permeability / Q000187:drug effects; D002374:Catalase / Q000494:pharmacology; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D005609:Free Radicals; D006801:Humans; D007958:Leukocyte Count; D008954:Models, Biological; D010100:Oxygen / Q000378:metabolism* / Q000633:toxicity; D011654:Pulmonary Edema / Q000209:etiology* / Q000473:pathology; D013482:Superoxide Dismutase / Q000494:pharmacology; D013890:Thiourea / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors
D005609:Free Radicals; D002374:Catalase; D013482:Superoxide Dismutase; D013890:Thiourea; D010100:Oxygen; C005277:alpha-naphthyl thiourea; D004121:Dimethyl Sulfoxide