The study by Rubanyi and Vanhoutte investigates the effects of oxygen-derived free radicals on the production and activity of endothelium-derived relaxing factor (EDRF) released by acetylcholine. They used a bioassay system with canine coronary arteries without endothelium to test the effects of superoxide dismutase (SOD) and catalase on EDRF. Key findings include: 1. **Superoxide Anions Inactivate EDRF**: SOD, when infused upstream of the femoral artery, caused relaxation in the bioassay ring, but this effect was inhibited by catalase. This suggests that superoxide anions inactivate EDRF. 2. **Hyperoxia Favors Inactivation**: Infusing acetylcholine relaxed the bioassay rings by releasing EDRF from the endothelium. When infused below the femoral artery, SOD and catalase augmented these relaxations, indicating that they protect EDRF from inactivation. 3. **SOD Prolongs EDRF Half-Life**: SOD doubled the half-life of EDRF, particularly when the oxygen content of the perfusate was lowered from 95% to 10%. This protective effect was more pronounced at lower oxygen levels. 4. **Oxygen Content and SOD**: Lowering the oxygen content from 95% to 10% increased the half-life of EDRF, suggesting that the inactivation of EDRF is influenced by the generation of superoxide anions, which can be reduced by SOD. 5. **Conclusion**: The study concludes that superoxide anions inactivate EDRF, and hyperoxia favors this inactivation. SOD protects EDRF by preventing its inactivation during transit, likely by reducing the concentration of superoxide anions or increasing the concentration of hydrogen peroxide.The study by Rubanyi and Vanhoutte investigates the effects of oxygen-derived free radicals on the production and activity of endothelium-derived relaxing factor (EDRF) released by acetylcholine. They used a bioassay system with canine coronary arteries without endothelium to test the effects of superoxide dismutase (SOD) and catalase on EDRF. Key findings include: 1. **Superoxide Anions Inactivate EDRF**: SOD, when infused upstream of the femoral artery, caused relaxation in the bioassay ring, but this effect was inhibited by catalase. This suggests that superoxide anions inactivate EDRF. 2. **Hyperoxia Favors Inactivation**: Infusing acetylcholine relaxed the bioassay rings by releasing EDRF from the endothelium. When infused below the femoral artery, SOD and catalase augmented these relaxations, indicating that they protect EDRF from inactivation. 3. **SOD Prolongs EDRF Half-Life**: SOD doubled the half-life of EDRF, particularly when the oxygen content of the perfusate was lowered from 95% to 10%. This protective effect was more pronounced at lower oxygen levels. 4. **Oxygen Content and SOD**: Lowering the oxygen content from 95% to 10% increased the half-life of EDRF, suggesting that the inactivation of EDRF is influenced by the generation of superoxide anions, which can be reduced by SOD. 5. **Conclusion**: The study concludes that superoxide anions inactivate EDRF, and hyperoxia favors this inactivation. SOD protects EDRF by preventing its inactivation during transit, likely by reducing the concentration of superoxide anions or increasing the concentration of hydrogen peroxide.