Circulation, Vol 83, 1015-1022, Copyright © 1991 by American Heart Association
T Iwamoto, T Miura, T Adachi, T Noto, T Ogawa, A Tsuchida and O Iimura
BACKGROUND. The limiting effect of ischemic preconditioning on infarct size
has been reported in canine hearts, which contain considerable amounts of
xanthine oxidase, a free radical-producing enzyme. Furthermore, a recent
study suggested that free radicals generated during preconditioning may
contribute to the cardioprotective effect of preconditioning. The present
study examined 1) whether preconditioning limits infarct size in rabbits,
which, like humans, lack myocardial xanthine oxidase and 2) whether the
cardioprotective effect of PC is mediated by free radicals. METHODS AND
RESULTS. A branch of the circumflex coronary artery in rabbits was occluded
for 30 minutes and then reperfused for 72 hours. Myocardial infarct size
and area at risk were determined by histology and fluorescent particles,
respectively. Five groups were studied: an untreated control group, a
preconditioned group (PC group), a high-dose superoxide dismutase
(SOD)-treated preconditioned group (high-dose SOD-PC group), a low-dose
SOD-treated preconditioned group (low-dose SOD-PC group), and a
SOD-plus-catalase- treated preconditioned group (SOD/CAT-PC group).
Preconditioning was performed with four episodes of 5 minutes of ischemia
and 5 minutes of reperfusion. The free radical scavengers (30,000 units/kg
SOD for high- dose SOD-PC group, 15,000 units/kg SOD for low-dose SOD-PC
group, and 30,000 units/kg SOD plus 55,000 units/kg catalase for SOD/CAT-PC
group) were infused intravenously over 60 minutes starting 20 minutes
before preconditioning. Infarct size as the percentage of area at risk was
45.1 +/- 3.5% (mean +/- SEM) in the control group (n = 11), 13.3 +/- 3.0%
in the PC group (n = 12), 9.7 +/- 1.8% in the high-dose SOD-PC group (n =
8), 11.9 +/- 2.2% in the low-dose SOD-PC group (n = 6), and 9.6 +/- 2.3% in
the SOD/CAT-PC group (n = 6) (p less than 0.05 versus control for the last
four values). The differences in infarct size as the percent of area at
risk among the PC, high-dose SOD-PC, low-dose SOD-PC, and SOD/CAT-PC groups
were not significant. CONCLUSION. Ischemic preconditioning delays ischemic
myocardial necrosis regardless of myocardial xanthine oxidase content. Free
radicals are unlikely to have a major role in the mechanism of the
preconditioning in rabbits.
ARTICLES
Myocardial infarct size-limiting effect of ischemic preconditioning was not attenuated by oxygen free-radical scavengers in the rabbit
Second Department of Internal Medicine, Sapporo Medical College, Japan.
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