Coronary Vasospasm After Angioplasty in Intact Dogs

a variety of mechanisms. This study assessed the role of the superoxide anion, the hydroxyl radical, and hydrogen peroxide in vasoconstriction and mural thrombosis after coronary artery angioplasty in intact dogs. Methods and Results. Injury was induced by inflation of a balloon catheter 50±6% above baseline arterial diameter; dogs were followed for 2 hours before death. Epicardial coronary diameters at arteriography and extent of thrombus deposition at serial histological sections were analyzed in controls (n=20) and in dogs pretreated with superoxide dismutase (SOD, a superoxide radical scavenger, n=10); other dogs were pretreated with the hydrogen peroxide scavenger catalase (n=8), the iron chelator deferoxamine (n=6), or the hydroxyl radical scavenger 1,3-dimethyl-2-thiourea (n=9). Angioplasty-induced injury was similar among groups. After angioplasty, control dogs exhibited localized and persistent vessel constriction, which was maximal at the initial 5 minutes (28.9+6.3% diameter decrease versus baseline). Corresponding arterial diameters of SOD-treated dogs were 24-69% larger (95% confidence interval, p<0.001) than controls at 5 minutes and, on average, 32% larger than controls thereafter (p<0.01). Vasoconstriction was not prevented by the other treatments. The SOD dose used accounted for inhibition of zymosan-stimulated blood cytochrome c reduction versus baseline (7+3 versus 30±6 nmol/min/106 cells, respectively,p=0.003); such inhibition occurred in no other group. Prevalence of mural thrombosis was similar among all groups, but large thrombi (>15% of lumen area) were absent in SOD-treated dogs, contrary to control group (p=0.028); other groups were similar to control. In the absence of injury, SOD alone induced