Circulation, Vol 83, 1705-1715, Copyright © 1991 by American Heart Association
FR Laurindo, PL da Luz, L Uint, TF Rocha, RG Jaeger and EA Lopes
BACKGROUND. Active oxygen species can influence vascular tone and platelet
activation through 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 less than 0.001) than controls at 5 minutes and, on average, 32% larger
than controls thereafter (p less than 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/10(6) cells, respectively, p =
0.003); such inhibition occurred in no other group. Prevalence of mural
thrombosis was similar among all groups, but large thrombi (greater than
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 no change in coronary diameter, coronary blood
flow, or platelet aggregation. CONCLUSIONS. These data provide evidence
implicating the superoxide radical in the genesis of vasoconstriction after
coronary angioplasty in vivo. Such effects seem to be independent of its
conversion to hydroxyl radicals and availability of hydrogen peroxide or
catalytic iron complexes.
ARTICLES
Evidence for superoxide radical-dependent coronary vasospasm after angioplasty in intact dogs
Division of Experimental Research, Faculdade de Medicina, Universidade de Sao Paulo, Brazil.
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