Superoxide dismutase decreases early reperfusion release of conjugated dienes following regional canine ischemia.

Oxygen radical-induced myocardial lipid peroxidation may cause injury during regional ischemia and reperfusion. However, in vivo detection of lipid peroxidation is difficult. Since conjugated dienes are lipid peroxidation products of unsaturated fatty acids, we evaluated the potential value of detection of these double-bonded fatty acids as a marker of oxygen radical injury. In seven untreated and five superoxide dismutase-treated anesthetized dogs exposed to 90 min of coronary occlusion and subsequent reperfusion, coronary sinus plasma draining the ischemic and reperfused region was assayed for dienes. Lipids were extracted and diene optical density measured at 233 nm wavelength. Superoxide dismutase (5 mg/kg, total dose) was infused into the left atrium during ischemia and the first 30 min of reperfusion. Coronary sinus diene optical density increased in untreated animals at 5 and 10 min of reperfusion (reperfusion optical density (x +/- SEM): 5 min = 1.49 +/- 0.20 absorbance units, 10 min = 1.36 +/- 0.06; both p less than 0.05 vs preocclusion optical density = 1.10 +/- 0.05 and 25 min reperfusion = 1.20 +/- 0.07). No increase in diene optical density occurred in superoxide dismutase-treated dogs. Myocardial lipid peroxidation products, as conjugated dienes, increased in coronary sinus plasma during early reperfusion and this increase was prevented by superoxide dismutase infusion.