Oleic-acid-induced lung injury in the rat. Failure of indomethacin treatment or complement depletion to ablate lung injury.
The purpose of this study was to establish a rat animal model of acute respiratory distress syndrome using the intravenous injection of oleic acid. Further, we attempted to inhibit the development of lung injury by pretreatment of the rats with indomethacin or cobra venom factor. Histologic evidence of lung injury was apparent within hours after the administration of a single intravenous injection of oleic acid. By 24 hours, interstitial and intraalveolar edema and hemorrhage were noted with vascular congestion and an extensive interstitial infiltrate. The lungs appeared virtually normal by 12 days, with no evidence of chronic lung injury. Multiple injections of oleic acid also did not progress into chronic pulmonary inflammation. Treatment of the rats with indomethacin or cobra venom factor had no effect on ablating acute lung injury. An animal model of adult respiratory distress syndrome is presented which does not progress to chronic lung injury.
D000818:Animals; D003176:Complement C3 / Q000032:analysis; D003165:Complement System Proteins / Q000172:deficiency*; D004195:Disease Models, Animal; D004546:Elapid Venoms / Q000627:therapeutic use; D007213:Indomethacin / Q000627:therapeutic use*; D007275:Injections, Intravenous; D008168:Lung / Q000276:immunology / Q000473:pathology; D008171:Lung Diseases / Q000139:chemically induced*; D008297:Male; D019301:Oleic Acid; D009829:Oleic Acids / Q000008:administration & dosage; D051381:Rats
D003176:Complement C3; D004546:Elapid Venoms; D009829:Oleic Acids; D019301:Oleic Acid; D003165:Complement System Proteins; D007213:Indomethacin